Structured Review

Cayman Chemical bml 111
<t>BML-111</t> alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Bml 111, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 93/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

2) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

3) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

4) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

5) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

6) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

7) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

8) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

9) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

10) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

11) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

12) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

13) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

14) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

15) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

16) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

17) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

18) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

19) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

20) Product Images from "Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling"

Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Journal: Respiratory Research

doi: 10.1186/s12931-018-0937-2

BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
Figure Legend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

Techniques Used: In Vivo, Staining

The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P
Figure Legend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

Techniques Used: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P
Figure Legend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

Techniques Used: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P
Figure Legend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot

BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P
Figure Legend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

Techniques Used: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P
Figure Legend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

Techniques Used: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

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    Cayman Chemical 7 trihydroxymethyl heptanoate
    <t>BML-111</t> alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
    7 Trihydroxymethyl Heptanoate, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/7 trihydroxymethyl heptanoate/product/Cayman Chemical
    Average 94 stars, based on 10 article reviews
    Price from $9.99 to $1999.99
    7 trihydroxymethyl heptanoate - by Bioz Stars, 2022-12
    94/100 stars
      Buy from Supplier

    90
    Cayman Chemical bml 111
    <t>BML-111</t> alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P
    Bml 111, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bml 111/product/Cayman Chemical
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bml 111 - by Bioz Stars, 2022-12
    90/100 stars
      Buy from Supplier

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    BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

    Article Snippet: As shown in Figs. a to c, the LC3-II/LC3-I ratio, LC3 and BECN1 levels were significantly lower, while SQSTM1/p62 level markedly higher in BML-111 + choloquine cells than in BML-111 alone cells, supporting the specific effects of BML-111 on autophagy.

    Techniques: In Vivo, Staining

    The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

    Article Snippet: As shown in Figs. a to c, the LC3-II/LC3-I ratio, LC3 and BECN1 levels were significantly lower, while SQSTM1/p62 level markedly higher in BML-111 + choloquine cells than in BML-111 alone cells, supporting the specific effects of BML-111 on autophagy.

    Techniques: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

    BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

    Article Snippet: As shown in Figs. a to c, the LC3-II/LC3-I ratio, LC3 and BECN1 levels were significantly lower, while SQSTM1/p62 level markedly higher in BML-111 + choloquine cells than in BML-111 alone cells, supporting the specific effects of BML-111 on autophagy.

    Techniques: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

    BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

    Article Snippet: As shown in Figs. a to c, the LC3-II/LC3-I ratio, LC3 and BECN1 levels were significantly lower, while SQSTM1/p62 level markedly higher in BML-111 + choloquine cells than in BML-111 alone cells, supporting the specific effects of BML-111 on autophagy.

    Techniques: Affinity Magnetic Separation, Expressing, Western Blot

    BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

    Article Snippet: As shown in Figs. a to c, the LC3-II/LC3-I ratio, LC3 and BECN1 levels were significantly lower, while SQSTM1/p62 level markedly higher in BML-111 + choloquine cells than in BML-111 alone cells, supporting the specific effects of BML-111 on autophagy.

    Techniques: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

    BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

    Article Snippet: As shown in Figs. a to c, the LC3-II/LC3-I ratio, LC3 and BECN1 levels were significantly lower, while SQSTM1/p62 level markedly higher in BML-111 + choloquine cells than in BML-111 alone cells, supporting the specific effects of BML-111 on autophagy.

    Techniques: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining

    BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 alleviated ALI in vivo. ALI model was established in rats by intratracheal instillation of LPS and rats were either not treated (ALI), or treated with vehicle (PBS + ALI) or BML-111 (BML-111 + ALI). As controls, rats not through ALI induction and treated with either vehicle (PBS) or BML-111 were used. a Upon sacrifice, the lung tissue from each group was examined by HE staining and assessed for ALI score. b The lung tissue was measured for wet/dry weight ratio and compared among different groups. n = 6, * P

    Article Snippet: To induce ALI-related damage, isolated AMs were treated with vehicle (PBS), LPS (Escherichia coli serotype 055:B5, 1 μg/mL; Sigma, St. Louis, MO, USA), BML-111 (100 nM; Cayman Chemical, Ann Arbor, MI, USA).

    Techniques: In Vivo, Staining

    The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: The benefits of BML-111 were associated with reduced inflammation and enhanced autophagy in vivo. Bronchoalveolar lavage was collected from rats of each group and the levels of TNF-α ( a ) and IL-6 ( b ) was measured using ELISA. AMs were isolated from rats of each group. c The expressions of TNF-α and IL-6 on the steady-state mRNA level were measured by RT-qPCR. d The expressions of BECN1, SQSTM1/p62, LC3-I, and LC3-II in isolated AM were examined by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right ( e ). n = 6, * P

    Article Snippet: To induce ALI-related damage, isolated AMs were treated with vehicle (PBS), LPS (Escherichia coli serotype 055:B5, 1 μg/mL; Sigma, St. Louis, MO, USA), BML-111 (100 nM; Cayman Chemical, Ann Arbor, MI, USA).

    Techniques: In Vivo, Enzyme-linked Immunosorbent Assay, Affinity Magnetic Separation, Isolation, Quantitative RT-PCR, Western Blot

    BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 inhibited LPS-induced apoptosis. AM were isolated from rats and treated with either vehicle (PBS), LPS (to induce ALI), BML-111, BML-111 + LPS. a At 24 h after the treatment, the cell viability was examined by MTT assay. b The apoptosis of cells was determined by flow cytometry following staining the cells with Annexin V and PI. c The expression of different apoptosis biomarkers, including cleaved-Caspase 3, cleaved-Caspase 8,cleaved-Caspase 9, cleaved-PARP, Bcl-2, and Bax was detected by Western blot. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. n = 3, * P

    Article Snippet: To induce ALI-related damage, isolated AMs were treated with vehicle (PBS), LPS (Escherichia coli serotype 055:B5, 1 μg/mL; Sigma, St. Louis, MO, USA), BML-111 (100 nM; Cayman Chemical, Ann Arbor, MI, USA).

    Techniques: Isolation, MTT Assay, Flow Cytometry, Cytometry, Staining, Expressing, Western Blot

    BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 elevated LC3-II level in AMs. AMs were treated with increasing concentrations of BML-111 for 2 h ( a ) or with 100 nM of BML-111 for indicated time periods ( b ). The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. n = 3, * P

    Article Snippet: To induce ALI-related damage, isolated AMs were treated with vehicle (PBS), LPS (Escherichia coli serotype 055:B5, 1 μg/mL; Sigma, St. Louis, MO, USA), BML-111 (100 nM; Cayman Chemical, Ann Arbor, MI, USA).

    Techniques: Affinity Magnetic Separation, Expressing, Western Blot

    BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 targeted MAPK1 pathway but mTOR-independent mechanism to induce autophagy. a The activation of MAPK1 and MAPK8 was detected by Western blot in AM treated as indicated. Representative Western blot image was shown on the left and the quantification of each protein level relative to that of the internal control (GAPDH) shown on the right. b AM were treated as indicated, in autophagy inhibitor MHY-1485 and mTOR inhibitor Rapamycin. LC3-II expression was examined by immunofluorescence (green signals). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the bottom and the percentage of LC3-II+ cells quantified and shown as histogram on the top. n = 3, * P

    Article Snippet: To induce ALI-related damage, isolated AMs were treated with vehicle (PBS), LPS (Escherichia coli serotype 055:B5, 1 μg/mL; Sigma, St. Louis, MO, USA), BML-111 (100 nM; Cayman Chemical, Ann Arbor, MI, USA).

    Techniques: Activation Assay, Western Blot, Expressing, Immunofluorescence, Staining

    BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

    Journal: Respiratory Research

    Article Title: Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

    doi: 10.1186/s12931-018-0937-2

    Figure Lengend Snippet: BML-111 elevated autophagy level in LPS-treated AM. AMs were treated as indicated. a The expression of LC3-I and LC3-II was examined by Western blot. Representative Western blot image was shown on the top and the LC3-II/LC3-I ratio shown on the bottom. b The expression of LC3-II in AM was detected by immunofluorescence (green signal). All cells were counter stained with DAPI (blue signal). Representative immunofluorescence images from indicated cells were shown on the left and the percentage of LC3-II+ cells quantified and shown as histogram on the right. c The expression of different autophagy and apoptosis biomarkers, including BECN1, SQSTM1/p62 was detected by Western blot. n = 3, * P

    Article Snippet: To induce ALI-related damage, isolated AMs were treated with vehicle (PBS), LPS (Escherichia coli serotype 055:B5, 1 μg/mL; Sigma, St. Louis, MO, USA), BML-111 (100 nM; Cayman Chemical, Ann Arbor, MI, USA).

    Techniques: Affinity Magnetic Separation, Expressing, Western Blot, Immunofluorescence, Staining