Structured Review

Cayman Chemical bml 111
Effect of <t>BML-111</t> on IL-1β, IL-6 and IL-8 expression in the serum of mice with sepsis. # P
Bml 111, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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bml 111 - by Bioz Stars, 2022-08
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Images

1) Product Images from "Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis"

Article Title: Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis

Journal: International Journal of Clinical and Experimental Medicine

doi:

Effect of BML-111 on IL-1β, IL-6 and IL-8 expression in the serum of mice with sepsis. # P
Figure Legend Snippet: Effect of BML-111 on IL-1β, IL-6 and IL-8 expression in the serum of mice with sepsis. # P

Techniques Used: Expressing, Mouse Assay

Effect of BML-111 on Wnt5a, FZD5 and CaMKIIδ expression in LPS-stimulated RAW 264.7 cells. Lane 1, PBS; lane 2, LPS; lane 3, BML-111 (1 ng/ml); lane 4, BML-111 (10 ng/ml); lane 5, BML-111 (100 ng/ml). * P
Figure Legend Snippet: Effect of BML-111 on Wnt5a, FZD5 and CaMKIIδ expression in LPS-stimulated RAW 264.7 cells. Lane 1, PBS; lane 2, LPS; lane 3, BML-111 (1 ng/ml); lane 4, BML-111 (10 ng/ml); lane 5, BML-111 (100 ng/ml). * P

Techniques Used: Expressing

Effect of BML-111 on Wnt5a/FZD5/CaMKII signaling in septic mice. Lane 1, sham; lane 2, sepsis; lane 3, BML-111. # P
Figure Legend Snippet: Effect of BML-111 on Wnt5a/FZD5/CaMKII signaling in septic mice. Lane 1, sham; lane 2, sepsis; lane 3, BML-111. # P

Techniques Used: Mouse Assay

Wnt5a/FZD5/CaMKII signaling mediates the effect of BML-111 on IL-1β, IL-6 and IL-8 expression in LPS-stimulated RAW 264.7 cells. # P
Figure Legend Snippet: Wnt5a/FZD5/CaMKII signaling mediates the effect of BML-111 on IL-1β, IL-6 and IL-8 expression in LPS-stimulated RAW 264.7 cells. # P

Techniques Used: Expressing

Expression of Wnt5a, FZD5 and CaMKIIδ in LPS-stimulated RAW 264.7 cells following treatment with BML-111 and transfection of Wnt5a-pcDNA3.1. Lane 1, LPS; lane 2, BML-111; lane 3, BML-111+Wnt5a. # P
Figure Legend Snippet: Expression of Wnt5a, FZD5 and CaMKIIδ in LPS-stimulated RAW 264.7 cells following treatment with BML-111 and transfection of Wnt5a-pcDNA3.1. Lane 1, LPS; lane 2, BML-111; lane 3, BML-111+Wnt5a. # P

Techniques Used: Expressing, Transfection

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 "BML-111 suppresses TGF-β1-induced lung fibroblast activation in vitro and decreases experimental pulmonary fibrosis in vivo"

Article Title: BML-111 suppresses TGF-β1-induced lung fibroblast activation in vitro and decreases experimental pulmonary fibrosis in vivo

Journal: International Journal of Molecular Medicine

doi: 10.3892/ijmm.2018.3914

BML-111 decreased TGF-β1-induced NIH3T3 cell α-SMA expression in a dose-dependent manner. (A) NIH3T3 cells express rs1 and (B) FPR2. Cells were pretreated with a vehicle (0.035% ethanol) or BML-111 (1, 10, 100, 200 and 500 nM) for 30 min and then treated with TGF-β1 (5 ng/ml) for 24 h. (C) The expression of α-SMA was assessed using western blotting and (D) quantified. Similar results were obtained from at least 3 sections. Data are expressed as the mean ± standard deviation. # P
Figure Legend Snippet: BML-111 decreased TGF-β1-induced NIH3T3 cell α-SMA expression in a dose-dependent manner. (A) NIH3T3 cells express rs1 and (B) FPR2. Cells were pretreated with a vehicle (0.035% ethanol) or BML-111 (1, 10, 100, 200 and 500 nM) for 30 min and then treated with TGF-β1 (5 ng/ml) for 24 h. (C) The expression of α-SMA was assessed using western blotting and (D) quantified. Similar results were obtained from at least 3 sections. Data are expressed as the mean ± standard deviation. # P

Techniques Used: Expressing, Western Blot, Standard Deviation

BML-111 treatment inhibited α-SMA expression and ECM deposition in lungs following BLM injection. Mice treated with 50 µ l saline (Sham group) or 2 mg/kg BLM (untreated group, BML-111 group and BOC-2 group) at day 0 were intraperitoneally injected with 1 ml saline (Sham and untreated group) or 1 mg/kg of BML-111 (BML-111 group and BOC-2 group) with or without 50 µ g/kg BOC-2 (BOC-2 group) every other day from day 0-21. Mice were sacrificed on day 21 and the expression of (A and B) α-SMA and (C) fibronectin was detected using western blotting. (D) Total collagen protein was measured using a Sircol collagen assay kit, and the content of (E) hydroxyproline was determined using a Hydroxyproline assay kit. Data are expressed as mean ± standard deviation. ## P
Figure Legend Snippet: BML-111 treatment inhibited α-SMA expression and ECM deposition in lungs following BLM injection. Mice treated with 50 µ l saline (Sham group) or 2 mg/kg BLM (untreated group, BML-111 group and BOC-2 group) at day 0 were intraperitoneally injected with 1 ml saline (Sham and untreated group) or 1 mg/kg of BML-111 (BML-111 group and BOC-2 group) with or without 50 µ g/kg BOC-2 (BOC-2 group) every other day from day 0-21. Mice were sacrificed on day 21 and the expression of (A and B) α-SMA and (C) fibronectin was detected using western blotting. (D) Total collagen protein was measured using a Sircol collagen assay kit, and the content of (E) hydroxyproline was determined using a Hydroxyproline assay kit. Data are expressed as mean ± standard deviation. ## P

Techniques Used: Expressing, Injection, Mouse Assay, Western Blot, Sircol Collagen Assay, Hydroxyproline Assay, Standard Deviation

BML-111 treatment improved mortality after BLM instillation. Mice received intratracheal injection of 50 µ l of saline (Sham group) or BLM 2 mg/kg (for untreated group, BML-111 group and BOC-2 group). Mice were treated intraperitoneally with the saline (for Sham group and untreated group) 1 ml or BML-111 (for BML-111 group and BOC-2 group) 1 mg/kg every other day from days 0 to 21, and BOC-2 group were given 50 µ g/kg BOC-2 30 min before the addition of BML-111, and monitored daily for survival. Data are analyzed by Kaplan-Meier method (n=10 for the Sham group and n=22 for the others). * P
Figure Legend Snippet: BML-111 treatment improved mortality after BLM instillation. Mice received intratracheal injection of 50 µ l of saline (Sham group) or BLM 2 mg/kg (for untreated group, BML-111 group and BOC-2 group). Mice were treated intraperitoneally with the saline (for Sham group and untreated group) 1 ml or BML-111 (for BML-111 group and BOC-2 group) 1 mg/kg every other day from days 0 to 21, and BOC-2 group were given 50 µ g/kg BOC-2 30 min before the addition of BML-111, and monitored daily for survival. Data are analyzed by Kaplan-Meier method (n=10 for the Sham group and n=22 for the others). * P

Techniques Used: Mouse Assay, Injection

BML-111 treatment mitigated the destruction of lung architecture and production of TGF-β1, TNF-α and IL-1β in BALF following BLM iniection. Mice were treated with 50 µ l saline (Sham group) or 2 mg/kg BLM (untreated group, BML-111 group and BOC-2 group) at day 0 were intraperitoneally administered with 1 ml of saline (Sham group and untreated group) or 1 mg/kg of BML-111 (BML-111 group and BOC-2 group) in the presence or absence of 50 µ g/kg BOC-2 (BOC-2 group) prior to the administration of BML-111. Mice were then sacrificed on day 21 and the extent of pulmonary injury and fibrosis were assessed using (A) H E and (B) Masson’s trichrome staining (magnification, ×100). (C) Fibrotic score was measured using the Ashcroft method. Levels of (D) TGF-β1, (E) TNF-α and (F) IL-1β in BALF were determined using ELISA. Data are expressed as mean ± standard deviation (n=8). ## P
Figure Legend Snippet: BML-111 treatment mitigated the destruction of lung architecture and production of TGF-β1, TNF-α and IL-1β in BALF following BLM iniection. Mice were treated with 50 µ l saline (Sham group) or 2 mg/kg BLM (untreated group, BML-111 group and BOC-2 group) at day 0 were intraperitoneally administered with 1 ml of saline (Sham group and untreated group) or 1 mg/kg of BML-111 (BML-111 group and BOC-2 group) in the presence or absence of 50 µ g/kg BOC-2 (BOC-2 group) prior to the administration of BML-111. Mice were then sacrificed on day 21 and the extent of pulmonary injury and fibrosis were assessed using (A) H E and (B) Masson’s trichrome staining (magnification, ×100). (C) Fibrotic score was measured using the Ashcroft method. Levels of (D) TGF-β1, (E) TNF-α and (F) IL-1β in BALF were determined using ELISA. Data are expressed as mean ± standard deviation (n=8). ## P

Techniques Used: Mouse Assay, Staining, Enzyme-linked Immunosorbent Assay, Standard Deviation

BML-111 suppressed TGF-β1-induced NIH3T3 cell activation. Cells were pretreated with a vehicle (0.035% ethanol) or BML-111 (200 nM) for 30 min in the absence or presence of BOC-2 (10 µ M; administered 30 min prior to BML-111 treatment) and then stimulated with TGF-β1 (5 ng/ml) for 24 h. (A) The protein expression of α-SMA and fibronectin and the results of the western blot analysis quantified for (B) α-SMA and (C) fibronectin; and (D) total collagen concentration and (E) cell viability were assessed. Data are presented as the mean ± standard deviation for three independent experiments. # P
Figure Legend Snippet: BML-111 suppressed TGF-β1-induced NIH3T3 cell activation. Cells were pretreated with a vehicle (0.035% ethanol) or BML-111 (200 nM) for 30 min in the absence or presence of BOC-2 (10 µ M; administered 30 min prior to BML-111 treatment) and then stimulated with TGF-β1 (5 ng/ml) for 24 h. (A) The protein expression of α-SMA and fibronectin and the results of the western blot analysis quantified for (B) α-SMA and (C) fibronectin; and (D) total collagen concentration and (E) cell viability were assessed. Data are presented as the mean ± standard deviation for three independent experiments. # P

Techniques Used: Activation Assay, Expressing, Western Blot, Concentration Assay, Standard Deviation

BML-111 inhibited TGF-β1-induced NIH3T3 cell Smad-dependent and Smad-independent signaling. NIH3T3 cells were stimulated using 5 ng/ml TGF-β1 in the absence or presence of 200 nM BML-111 (added 30 min prior to experimentation). Levels of (A) Smad2/3 and phosphorylated (B) Smad2/(C) Smad3 were assessed. (D) ERK and (E) phosphorylated ERK, (F) Aktand (G) phosphorylated Aktwere also analyzed using western blotting, 24 h following cell stimulation. The figures are representative results of three independent experiments. Data are expressed as mean ± standard deviation. ## P
Figure Legend Snippet: BML-111 inhibited TGF-β1-induced NIH3T3 cell Smad-dependent and Smad-independent signaling. NIH3T3 cells were stimulated using 5 ng/ml TGF-β1 in the absence or presence of 200 nM BML-111 (added 30 min prior to experimentation). Levels of (A) Smad2/3 and phosphorylated (B) Smad2/(C) Smad3 were assessed. (D) ERK and (E) phosphorylated ERK, (F) Aktand (G) phosphorylated Aktwere also analyzed using western blotting, 24 h following cell stimulation. The figures are representative results of three independent experiments. Data are expressed as mean ± standard deviation. ## P

Techniques Used: Western Blot, Cell Stimulation, Standard Deviation

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 "Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis"

Article Title: Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis

Journal: International Journal of Clinical and Experimental Medicine

doi:

Effect of BML-111 on IL-1β, IL-6 and IL-8 expression in the serum of mice with sepsis. # P
Figure Legend Snippet: Effect of BML-111 on IL-1β, IL-6 and IL-8 expression in the serum of mice with sepsis. # P

Techniques Used: Expressing, Mouse Assay

Effect of BML-111 on Wnt5a, FZD5 and CaMKIIδ expression in LPS-stimulated RAW 264.7 cells. Lane 1, PBS; lane 2, LPS; lane 3, BML-111 (1 ng/ml); lane 4, BML-111 (10 ng/ml); lane 5, BML-111 (100 ng/ml). * P
Figure Legend Snippet: Effect of BML-111 on Wnt5a, FZD5 and CaMKIIδ expression in LPS-stimulated RAW 264.7 cells. Lane 1, PBS; lane 2, LPS; lane 3, BML-111 (1 ng/ml); lane 4, BML-111 (10 ng/ml); lane 5, BML-111 (100 ng/ml). * P

Techniques Used: Expressing

Effect of BML-111 on Wnt5a/FZD5/CaMKII signaling in septic mice. Lane 1, sham; lane 2, sepsis; lane 3, BML-111. # P
Figure Legend Snippet: Effect of BML-111 on Wnt5a/FZD5/CaMKII signaling in septic mice. Lane 1, sham; lane 2, sepsis; lane 3, BML-111. # P

Techniques Used: Mouse Assay

Wnt5a/FZD5/CaMKII signaling mediates the effect of BML-111 on IL-1β, IL-6 and IL-8 expression in LPS-stimulated RAW 264.7 cells. # P
Figure Legend Snippet: Wnt5a/FZD5/CaMKII signaling mediates the effect of BML-111 on IL-1β, IL-6 and IL-8 expression in LPS-stimulated RAW 264.7 cells. # P

Techniques Used: Expressing

Expression of Wnt5a, FZD5 and CaMKIIδ in LPS-stimulated RAW 264.7 cells following treatment with BML-111 and transfection of Wnt5a-pcDNA3.1. Lane 1, LPS; lane 2, BML-111; lane 3, BML-111+Wnt5a. # P
Figure Legend Snippet: Expression of Wnt5a, FZD5 and CaMKIIδ in LPS-stimulated RAW 264.7 cells following treatment with BML-111 and transfection of Wnt5a-pcDNA3.1. Lane 1, LPS; lane 2, BML-111; lane 3, BML-111+Wnt5a. # P

Techniques Used: Expressing, Transfection

7) Product Images from "Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis"

Article Title: Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis

Journal: International Journal of Clinical and Experimental Medicine

doi:

Effect of BML-111 on IL-1β, IL-6 and IL-8 expression in the serum of mice with sepsis. # P
Figure Legend Snippet: Effect of BML-111 on IL-1β, IL-6 and IL-8 expression in the serum of mice with sepsis. # P

Techniques Used: Expressing, Mouse Assay

Effect of BML-111 on Wnt5a, FZD5 and CaMKIIδ expression in LPS-stimulated RAW 264.7 cells. Lane 1, PBS; lane 2, LPS; lane 3, BML-111 (1 ng/ml); lane 4, BML-111 (10 ng/ml); lane 5, BML-111 (100 ng/ml). * P
Figure Legend Snippet: Effect of BML-111 on Wnt5a, FZD5 and CaMKIIδ expression in LPS-stimulated RAW 264.7 cells. Lane 1, PBS; lane 2, LPS; lane 3, BML-111 (1 ng/ml); lane 4, BML-111 (10 ng/ml); lane 5, BML-111 (100 ng/ml). * P

Techniques Used: Expressing

Effect of BML-111 on Wnt5a/FZD5/CaMKII signaling in septic mice. Lane 1, sham; lane 2, sepsis; lane 3, BML-111. # P
Figure Legend Snippet: Effect of BML-111 on Wnt5a/FZD5/CaMKII signaling in septic mice. Lane 1, sham; lane 2, sepsis; lane 3, BML-111. # P

Techniques Used: Mouse Assay

Wnt5a/FZD5/CaMKII signaling mediates the effect of BML-111 on IL-1β, IL-6 and IL-8 expression in LPS-stimulated RAW 264.7 cells. # P
Figure Legend Snippet: Wnt5a/FZD5/CaMKII signaling mediates the effect of BML-111 on IL-1β, IL-6 and IL-8 expression in LPS-stimulated RAW 264.7 cells. # P

Techniques Used: Expressing

Expression of Wnt5a, FZD5 and CaMKIIδ in LPS-stimulated RAW 264.7 cells following treatment with BML-111 and transfection of Wnt5a-pcDNA3.1. Lane 1, LPS; lane 2, BML-111; lane 3, BML-111+Wnt5a. # P
Figure Legend Snippet: Expression of Wnt5a, FZD5 and CaMKIIδ in LPS-stimulated RAW 264.7 cells following treatment with BML-111 and transfection of Wnt5a-pcDNA3.1. Lane 1, LPS; lane 2, BML-111; lane 3, BML-111+Wnt5a. # P

Techniques Used: Expressing, Transfection

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    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
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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: After treating the cells with vehicle, LPS, BML-111, or LPS + BML-111 for 24 h, 20 μL of MTT agent (5 mg/mL) was added into each well and incubated at 37 °C for a further 4 h. After gentle shaking and removal of the supernatant, dimethyl sulfoxide (DMSO; 150 μL/well) was added into each well to dissolve the formazan crystals.

    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: After treating the cells with vehicle, LPS, BML-111, or LPS + BML-111 for 24 h, 20 μL of MTT agent (5 mg/mL) was added into each well and incubated at 37 °C for a further 4 h. After gentle shaking and removal of the supernatant, dimethyl sulfoxide (DMSO; 150 μL/well) was added into each well to dissolve the formazan crystals.

    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: After treating the cells with vehicle, LPS, BML-111, or LPS + BML-111 for 24 h, 20 μL of MTT agent (5 mg/mL) was added into each well and incubated at 37 °C for a further 4 h. After gentle shaking and removal of the supernatant, dimethyl sulfoxide (DMSO; 150 μL/well) was added into each well to dissolve the formazan crystals.

    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: After treating the cells with vehicle, LPS, BML-111, or LPS + BML-111 for 24 h, 20 μL of MTT agent (5 mg/mL) was added into each well and incubated at 37 °C for a further 4 h. After gentle shaking and removal of the supernatant, dimethyl sulfoxide (DMSO; 150 μL/well) was added into each well to dissolve the formazan crystals.

    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: After treating the cells with vehicle, LPS, BML-111, or LPS + BML-111 for 24 h, 20 μL of MTT agent (5 mg/mL) was added into each well and incubated at 37 °C for a further 4 h. After gentle shaking and removal of the supernatant, dimethyl sulfoxide (DMSO; 150 μL/well) was added into each well to dissolve the formazan crystals.

    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: After treating the cells with vehicle, LPS, BML-111, or LPS + BML-111 for 24 h, 20 μL of MTT agent (5 mg/mL) was added into each well and incubated at 37 °C for a further 4 h. After gentle shaking and removal of the supernatant, dimethyl sulfoxide (DMSO; 150 μL/well) was added into each well to dissolve the formazan crystals.

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

    Effect of BML-111 on IL-1β, IL-6 and IL-8 expression in the serum of mice with sepsis. # P

    Journal: International Journal of Clinical and Experimental Medicine

    Article Title: Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis

    doi:

    Figure Lengend Snippet: Effect of BML-111 on IL-1β, IL-6 and IL-8 expression in the serum of mice with sepsis. # P

    Article Snippet: BML-111 also suppressed airway inflammation of ovalbumin-immunized mice.

    Techniques: Expressing, Mouse Assay

    Effect of BML-111 on Wnt5a, FZD5 and CaMKIIδ expression in LPS-stimulated RAW 264.7 cells. Lane 1, PBS; lane 2, LPS; lane 3, BML-111 (1 ng/ml); lane 4, BML-111 (10 ng/ml); lane 5, BML-111 (100 ng/ml). * P

    Journal: International Journal of Clinical and Experimental Medicine

    Article Title: Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis

    doi:

    Figure Lengend Snippet: Effect of BML-111 on Wnt5a, FZD5 and CaMKIIδ expression in LPS-stimulated RAW 264.7 cells. Lane 1, PBS; lane 2, LPS; lane 3, BML-111 (1 ng/ml); lane 4, BML-111 (10 ng/ml); lane 5, BML-111 (100 ng/ml). * P

    Article Snippet: BML-111 also suppressed airway inflammation of ovalbumin-immunized mice.

    Techniques: Expressing

    Effect of BML-111 on Wnt5a/FZD5/CaMKII signaling in septic mice. Lane 1, sham; lane 2, sepsis; lane 3, BML-111. # P

    Journal: International Journal of Clinical and Experimental Medicine

    Article Title: Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis

    doi:

    Figure Lengend Snippet: Effect of BML-111 on Wnt5a/FZD5/CaMKII signaling in septic mice. Lane 1, sham; lane 2, sepsis; lane 3, BML-111. # P

    Article Snippet: BML-111 also suppressed airway inflammation of ovalbumin-immunized mice.

    Techniques: Mouse Assay

    Wnt5a/FZD5/CaMKII signaling mediates the effect of BML-111 on IL-1β, IL-6 and IL-8 expression in LPS-stimulated RAW 264.7 cells. # P

    Journal: International Journal of Clinical and Experimental Medicine

    Article Title: Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis

    doi:

    Figure Lengend Snippet: Wnt5a/FZD5/CaMKII signaling mediates the effect of BML-111 on IL-1β, IL-6 and IL-8 expression in LPS-stimulated RAW 264.7 cells. # P

    Article Snippet: BML-111 also suppressed airway inflammation of ovalbumin-immunized mice.

    Techniques: Expressing

    Expression of Wnt5a, FZD5 and CaMKIIδ in LPS-stimulated RAW 264.7 cells following treatment with BML-111 and transfection of Wnt5a-pcDNA3.1. Lane 1, LPS; lane 2, BML-111; lane 3, BML-111+Wnt5a. # P

    Journal: International Journal of Clinical and Experimental Medicine

    Article Title: Wnt5a/FZD5/CaMKII signaling pathway mediates the effect of BML-111 on inflammatory reactions in sepsis

    doi:

    Figure Lengend Snippet: Expression of Wnt5a, FZD5 and CaMKIIδ in LPS-stimulated RAW 264.7 cells following treatment with BML-111 and transfection of Wnt5a-pcDNA3.1. Lane 1, LPS; lane 2, BML-111; lane 3, BML-111+Wnt5a. # P

    Article Snippet: BML-111 also suppressed airway inflammation of ovalbumin-immunized mice.

    Techniques: Expressing, Transfection

    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: When monitoring AMs for apoptosis by dual staining with Annexin V and PI, we observed that LPS potently induced apoptosis, increased apoptosis rate from an average of 9.02% in control PBS-treated cells to approximately 33.28% in LPS-treated cells (P < 0.05); the latter was partially yet significantly reduced by the pre-treatment of cells with the lipoxin A4 agonist BML-111 (P < 0.05, comparing LPS- to BML-111 + LPS-treated cells), even though BML-111 alone did not significantly affect cellular apoptosis (P > 0.05, comparing control- to BML-111-treated cells; Fig. b).

    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: When monitoring AMs for apoptosis by dual staining with Annexin V and PI, we observed that LPS potently induced apoptosis, increased apoptosis rate from an average of 9.02% in control PBS-treated cells to approximately 33.28% in LPS-treated cells (P < 0.05); the latter was partially yet significantly reduced by the pre-treatment of cells with the lipoxin A4 agonist BML-111 (P < 0.05, comparing LPS- to BML-111 + LPS-treated cells), even though BML-111 alone did not significantly affect cellular apoptosis (P > 0.05, comparing control- to BML-111-treated cells; Fig. b).

    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: When monitoring AMs for apoptosis by dual staining with Annexin V and PI, we observed that LPS potently induced apoptosis, increased apoptosis rate from an average of 9.02% in control PBS-treated cells to approximately 33.28% in LPS-treated cells (P < 0.05); the latter was partially yet significantly reduced by the pre-treatment of cells with the lipoxin A4 agonist BML-111 (P < 0.05, comparing LPS- to BML-111 + LPS-treated cells), even though BML-111 alone did not significantly affect cellular apoptosis (P > 0.05, comparing control- to BML-111-treated cells; Fig. b).

    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: When monitoring AMs for apoptosis by dual staining with Annexin V and PI, we observed that LPS potently induced apoptosis, increased apoptosis rate from an average of 9.02% in control PBS-treated cells to approximately 33.28% in LPS-treated cells (P < 0.05); the latter was partially yet significantly reduced by the pre-treatment of cells with the lipoxin A4 agonist BML-111 (P < 0.05, comparing LPS- to BML-111 + LPS-treated cells), even though BML-111 alone did not significantly affect cellular apoptosis (P > 0.05, comparing control- to BML-111-treated cells; Fig. b).

    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: When monitoring AMs for apoptosis by dual staining with Annexin V and PI, we observed that LPS potently induced apoptosis, increased apoptosis rate from an average of 9.02% in control PBS-treated cells to approximately 33.28% in LPS-treated cells (P < 0.05); the latter was partially yet significantly reduced by the pre-treatment of cells with the lipoxin A4 agonist BML-111 (P < 0.05, comparing LPS- to BML-111 + LPS-treated cells), even though BML-111 alone did not significantly affect cellular apoptosis (P > 0.05, comparing control- to BML-111-treated cells; Fig. b).

    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: When monitoring AMs for apoptosis by dual staining with Annexin V and PI, we observed that LPS potently induced apoptosis, increased apoptosis rate from an average of 9.02% in control PBS-treated cells to approximately 33.28% in LPS-treated cells (P < 0.05); the latter was partially yet significantly reduced by the pre-treatment of cells with the lipoxin A4 agonist BML-111 (P < 0.05, comparing LPS- to BML-111 + LPS-treated cells), even though BML-111 alone did not significantly affect cellular apoptosis (P > 0.05, comparing control- to BML-111-treated cells; Fig. b).

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