elisa kit  (Boster Bio)


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    Structured Review

    Boster Bio elisa kit
    Therapeutical effect of NLRP3 knockdown on NLRP3 inflammasome activation, phenotypic transformation, vascular remodeling and hypertension in SHR. The measurements were made 2 weeks after transfection. ( a ) Relative protein expressions of NLRP3, procaspase-1, caspase-1, pro-IL-1 β and IL-1 β . ( b ) Ratio of caspase-1 to procaspase-1 and ratio of IL-1 β to pro-IL-1 β . ( c ) IL-1 β levels measured with <t>enzyme-linked</t> <t>immunosorbent</t> <t>assay.</t> ( d ) Relative protein expressions of OPN, α -SMA, SM22 α and PCNA. ( e ) Representative images showing EdU-positive cells measured with EdU incorporation assay. Blue fluorescence shows cell nuclei and red fluorescence stands for cells with DNA synthesis. ( f ) Bar graph showing the percentage of EdU-positive cells. ( g ) Representative sections of thoracic aortas with Masson staining. ( h ) Media thickness (M), lumen diameter (L) and the ratio of M to L of aorta. Values are mean±S.E. * P
    Elisa Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 40 article reviews
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    elisa kit - by Bioz Stars, 2022-10
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    Images

    1) Product Images from "NLRP3 inflammasome activation contributes to VSMC phenotypic transformation and proliferation in hypertension"

    Article Title: NLRP3 inflammasome activation contributes to VSMC phenotypic transformation and proliferation in hypertension

    Journal: Cell Death & Disease

    doi: 10.1038/cddis.2017.470

    Therapeutical effect of NLRP3 knockdown on NLRP3 inflammasome activation, phenotypic transformation, vascular remodeling and hypertension in SHR. The measurements were made 2 weeks after transfection. ( a ) Relative protein expressions of NLRP3, procaspase-1, caspase-1, pro-IL-1 β and IL-1 β . ( b ) Ratio of caspase-1 to procaspase-1 and ratio of IL-1 β to pro-IL-1 β . ( c ) IL-1 β levels measured with enzyme-linked immunosorbent assay. ( d ) Relative protein expressions of OPN, α -SMA, SM22 α and PCNA. ( e ) Representative images showing EdU-positive cells measured with EdU incorporation assay. Blue fluorescence shows cell nuclei and red fluorescence stands for cells with DNA synthesis. ( f ) Bar graph showing the percentage of EdU-positive cells. ( g ) Representative sections of thoracic aortas with Masson staining. ( h ) Media thickness (M), lumen diameter (L) and the ratio of M to L of aorta. Values are mean±S.E. * P
    Figure Legend Snippet: Therapeutical effect of NLRP3 knockdown on NLRP3 inflammasome activation, phenotypic transformation, vascular remodeling and hypertension in SHR. The measurements were made 2 weeks after transfection. ( a ) Relative protein expressions of NLRP3, procaspase-1, caspase-1, pro-IL-1 β and IL-1 β . ( b ) Ratio of caspase-1 to procaspase-1 and ratio of IL-1 β to pro-IL-1 β . ( c ) IL-1 β levels measured with enzyme-linked immunosorbent assay. ( d ) Relative protein expressions of OPN, α -SMA, SM22 α and PCNA. ( e ) Representative images showing EdU-positive cells measured with EdU incorporation assay. Blue fluorescence shows cell nuclei and red fluorescence stands for cells with DNA synthesis. ( f ) Bar graph showing the percentage of EdU-positive cells. ( g ) Representative sections of thoracic aortas with Masson staining. ( h ) Media thickness (M), lumen diameter (L) and the ratio of M to L of aorta. Values are mean±S.E. * P

    Techniques Used: Activation Assay, Transformation Assay, Transfection, Enzyme-linked Immunosorbent Assay, Fluorescence, DNA Synthesis, Staining

    NLRP3 inflammasome activation and phenotypic transformation in the aortic media of WKY and SHR. ( a ) Immunofluorescence double staining showing the overlap of NLRP3 (red) and SM- α actin (green) in aorta. Nuclei were stained by DAPI (blue). ( b ) Relative mRNA levels of NLRP3, ASC, caspase-1 and IL-1 β in media of aorta. ( c ) Relative protein expressions of NLRP3, ASC, procaspase-1, caspase-1, pro-IL-1 β and IL-1 β in media of aorta. ( d ) Ratio of caspase-1 to procaspase-1 and ratio of IL-1 β to pro-IL-1 β . ( e ) IL-1 β levels measured with enzyme-linked immunosorbent assay. ( f ) Expressions of synthetic protein (OPN) and contractile proteins ( α -SMA, SM22 α ) in media of aorta. Values are mean±S.E. * P
    Figure Legend Snippet: NLRP3 inflammasome activation and phenotypic transformation in the aortic media of WKY and SHR. ( a ) Immunofluorescence double staining showing the overlap of NLRP3 (red) and SM- α actin (green) in aorta. Nuclei were stained by DAPI (blue). ( b ) Relative mRNA levels of NLRP3, ASC, caspase-1 and IL-1 β in media of aorta. ( c ) Relative protein expressions of NLRP3, ASC, procaspase-1, caspase-1, pro-IL-1 β and IL-1 β in media of aorta. ( d ) Ratio of caspase-1 to procaspase-1 and ratio of IL-1 β to pro-IL-1 β . ( e ) IL-1 β levels measured with enzyme-linked immunosorbent assay. ( f ) Expressions of synthetic protein (OPN) and contractile proteins ( α -SMA, SM22 α ) in media of aorta. Values are mean±S.E. * P

    Techniques Used: Activation Assay, Transformation Assay, Immunofluorescence, Double Staining, Staining, Enzyme-linked Immunosorbent Assay

    2) Product Images from "Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus"

    Article Title: Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus

    Journal: Translational Neuroscience

    doi: 10.1515/tnsci-2020-0010

    Identification of PHH rat model. (a) Results of HE and Masson staining in the brain tissues showed that the cerebral cortex was compressed and thinned, and the cells of subcutaneous brain tissue were swollen and deformed. (b) Transmission electron microscopy of arachnoid in PHH rats: Figure I shows the longitudinal collagen fibers in the arachnoid, presenting dense collagen fibers and complete arachnoid fibrosis. The red arrow shows fibroblasts, suggesting that fibrosis may occur in arachnoid cells. Figure II shows the horizontal collagen fibers in the arachnoid of the rats, presenting dense collagen fibers and arachnoid fibrosis. (c) Tomography of brain tissues in PHH rats. Figure II is a partial magnification schematic diagram of the red box in Figure I, presenting obvious fibrosis in the arachnoid and subarachnoid space. The subarachnoid space was filled with collagen fibers, and the pores of the arachnoid cerebellum were narrowed. (d) Detection of activated TGF-β1 in the CSF by ELISA (** P
    Figure Legend Snippet: Identification of PHH rat model. (a) Results of HE and Masson staining in the brain tissues showed that the cerebral cortex was compressed and thinned, and the cells of subcutaneous brain tissue were swollen and deformed. (b) Transmission electron microscopy of arachnoid in PHH rats: Figure I shows the longitudinal collagen fibers in the arachnoid, presenting dense collagen fibers and complete arachnoid fibrosis. The red arrow shows fibroblasts, suggesting that fibrosis may occur in arachnoid cells. Figure II shows the horizontal collagen fibers in the arachnoid of the rats, presenting dense collagen fibers and arachnoid fibrosis. (c) Tomography of brain tissues in PHH rats. Figure II is a partial magnification schematic diagram of the red box in Figure I, presenting obvious fibrosis in the arachnoid and subarachnoid space. The subarachnoid space was filled with collagen fibers, and the pores of the arachnoid cerebellum were narrowed. (d) Detection of activated TGF-β1 in the CSF by ELISA (** P

    Techniques Used: Staining, Transmission Assay, Electron Microscopy, Tomography, Enzyme-linked Immunosorbent Assay

    3) Product Images from "Bacillus Calmette-Guerin alleviates airway inflammation and remodeling by preventing TGF-β1 induced epithelial–mesenchymal transition"

    Article Title: Bacillus Calmette-Guerin alleviates airway inflammation and remodeling by preventing TGF-β1 induced epithelial–mesenchymal transition

    Journal: Human Vaccines & Immunotherapeutics

    doi: 10.1080/21645515.2017.1313366

    BCG decreased the levels of TGF-β1 in BALF and sera in a rat model of asthma as analyzed by ELISA. Values are expressed as mean ± SD (n = 8) Significant at: # P
    Figure Legend Snippet: BCG decreased the levels of TGF-β1 in BALF and sera in a rat model of asthma as analyzed by ELISA. Values are expressed as mean ± SD (n = 8) Significant at: # P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    4) Product Images from "Curcumin Modulates the Crosstalk Between Macrophages and Bone Mesenchymal Stem Cells to Ameliorate Osteogenesis"

    Article Title: Curcumin Modulates the Crosstalk Between Macrophages and Bone Mesenchymal Stem Cells to Ameliorate Osteogenesis

    Journal: Frontiers in Cell and Developmental Biology

    doi: 10.3389/fcell.2021.634650

    (A,B) Concentrations of IL-1β, TNF-α, IL-4, and IL-10 in the cell supernatant measured by ELISA. (C,D) Gene expressions of the pro-inflammatory cytokines IL-1β and TNF-α, and the anti-inflammatory cytokines IL-4 and IL-10 measured by real-time PCR. ∗∗ P
    Figure Legend Snippet: (A,B) Concentrations of IL-1β, TNF-α, IL-4, and IL-10 in the cell supernatant measured by ELISA. (C,D) Gene expressions of the pro-inflammatory cytokines IL-1β and TNF-α, and the anti-inflammatory cytokines IL-4 and IL-10 measured by real-time PCR. ∗∗ P

    Techniques Used: Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction

    5) Product Images from "FASN promotes lymph node metastasis in cervical cancer via cholesterol reprogramming and lymphangiogenesis"

    Article Title: FASN promotes lymph node metastasis in cervical cancer via cholesterol reprogramming and lymphangiogenesis

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-022-04926-2

    FASN induces lymphangiogenesis by secreting PDGF-AA and IGFBP-3. A Human angiogenesis array kit results showed five differentiated angiogenesis-related factors in the HeLa-sh-Ctrl and HeLa-sh-FASN groups. Each group contained three replicates of the culture supernatant mixture. B Heatmap of these five factors in A based on pixel analysis. C , D ELISA validation of MMP-9, Angiogenin, VEGF, PDGF-AA, and IGFBP-3 in the culture supernatant of the FASN-shRNA-treated HeLa and CaSki cells. E ELISA validation of MMP-9, Angiogenin, VEGF, PDGF-AA, and IGFBP-3 in the culture supernatant of the C33A-FASN-OE and C33A-vector groups. F , G Rescue experiments showed that the addition of PDGF-AA and IGFBP-3 could rescue the impaired effect of FASN knockdown on lymphangiogenesis. Tube length in tube formation assays was quantified. * P
    Figure Legend Snippet: FASN induces lymphangiogenesis by secreting PDGF-AA and IGFBP-3. A Human angiogenesis array kit results showed five differentiated angiogenesis-related factors in the HeLa-sh-Ctrl and HeLa-sh-FASN groups. Each group contained three replicates of the culture supernatant mixture. B Heatmap of these five factors in A based on pixel analysis. C , D ELISA validation of MMP-9, Angiogenin, VEGF, PDGF-AA, and IGFBP-3 in the culture supernatant of the FASN-shRNA-treated HeLa and CaSki cells. E ELISA validation of MMP-9, Angiogenin, VEGF, PDGF-AA, and IGFBP-3 in the culture supernatant of the C33A-FASN-OE and C33A-vector groups. F , G Rescue experiments showed that the addition of PDGF-AA and IGFBP-3 could rescue the impaired effect of FASN knockdown on lymphangiogenesis. Tube length in tube formation assays was quantified. * P

    Techniques Used: Enzyme-linked Immunosorbent Assay, shRNA, Plasmid Preparation

    6) Product Images from "Pilose Antler Peptide-3.2KD Ameliorates Adriamycin-Induced Myocardial Injury Through TGF-β/SMAD Signaling Pathway"

    Article Title: Pilose Antler Peptide-3.2KD Ameliorates Adriamycin-Induced Myocardial Injury Through TGF-β/SMAD Signaling Pathway

    Journal: Frontiers in Cardiovascular Medicine

    doi: 10.3389/fcvm.2021.659643

    PAP-3.2KD regulated the expression levels of Bcl-2, Bax, and caspase-3 in ADR-induced rats. The concentrations of Bcl-2 (A) , Bax (B) and Caspase-3 (C) in cardiac tissue were determined by ELISA. Data were presented as Mean ± standard error of mean ( n = 10). (D) The protein expression levels of Bcl-2, Bax and Caspase-3 were determined by western blotting. (E) Statistical analysis for expression levels of relative protein in (D) , GAPDH protein levels as control. Data were presented as Mean ± standard error of mean ( n = 3). ## P
    Figure Legend Snippet: PAP-3.2KD regulated the expression levels of Bcl-2, Bax, and caspase-3 in ADR-induced rats. The concentrations of Bcl-2 (A) , Bax (B) and Caspase-3 (C) in cardiac tissue were determined by ELISA. Data were presented as Mean ± standard error of mean ( n = 10). (D) The protein expression levels of Bcl-2, Bax and Caspase-3 were determined by western blotting. (E) Statistical analysis for expression levels of relative protein in (D) , GAPDH protein levels as control. Data were presented as Mean ± standard error of mean ( n = 3). ## P

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, Western Blot

    7) Product Images from "Mechanism of QingHuaZhiXie Prescription Regulating TLR4-IECs Pathway in the Intervention of Diarrhea Predominant Irritable Bowel Syndrome"

    Article Title: Mechanism of QingHuaZhiXie Prescription Regulating TLR4-IECs Pathway in the Intervention of Diarrhea Predominant Irritable Bowel Syndrome

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    doi: 10.1155/2021/5792130

    Effect of QingHuaZhiXie prescription on expression level of inflammatory factors and MPO activity. (a) Transcription levels of TNF- α and IFN- γ based on RT-qPCR analysis. (b) Expression levels of TNF- α and IFN- γ based on ELISA analysis. (c) Examined MPO activity through immunohistochemical analysis. ∗∗∗ P
    Figure Legend Snippet: Effect of QingHuaZhiXie prescription on expression level of inflammatory factors and MPO activity. (a) Transcription levels of TNF- α and IFN- γ based on RT-qPCR analysis. (b) Expression levels of TNF- α and IFN- γ based on ELISA analysis. (c) Examined MPO activity through immunohistochemical analysis. ∗∗∗ P

    Techniques Used: Expressing, Activity Assay, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Immunohistochemistry

    8) Product Images from "Hyperleptinemia directly affects testicular maturation at different sexual stages in mice, and suppressor of cytokine signaling 3 is involved in this process"

    Article Title: Hyperleptinemia directly affects testicular maturation at different sexual stages in mice, and suppressor of cytokine signaling 3 is involved in this process

    Journal: Reproductive Biology and Endocrinology : RB & E

    doi: 10.1186/1477-7827-12-15

    Change in testosterone and offspring was recovered partly by decreasing leptin concentration by the withdrawal of MSG treatment. Mice were treated with MSG from d0 to d14 or d28, and then injected with NS instead of MSG to d56; these groups are called 14MSG-d56 and 28MSG-d56, respectively. The leptin level of the mouse plasma was measured by ELISA (A) . Testosterone level of plasma was detected by EIA (B) . The methods to measure the testicular weight and volume (C) were described in the Materials and Methods. The total number of offspring was divided by the number of mated female mice to obtain the average number of offspring for each female mouse (D) . The means were compared using a one-way analysis of variance followed by Student-Newman-Keuls test to conduct multiple comparisons. *, p
    Figure Legend Snippet: Change in testosterone and offspring was recovered partly by decreasing leptin concentration by the withdrawal of MSG treatment. Mice were treated with MSG from d0 to d14 or d28, and then injected with NS instead of MSG to d56; these groups are called 14MSG-d56 and 28MSG-d56, respectively. The leptin level of the mouse plasma was measured by ELISA (A) . Testosterone level of plasma was detected by EIA (B) . The methods to measure the testicular weight and volume (C) were described in the Materials and Methods. The total number of offspring was divided by the number of mated female mice to obtain the average number of offspring for each female mouse (D) . The means were compared using a one-way analysis of variance followed by Student-Newman-Keuls test to conduct multiple comparisons. *, p

    Techniques Used: Concentration Assay, Mouse Assay, Injection, Enzyme-linked Immunosorbent Assay

    9) Product Images from "Metformin attenuates motility, contraction, and fibrogenic response of hepatic stellate cells in vivo and in vitro by activating AMP-activated protein kinase"

    Article Title: Metformin attenuates motility, contraction, and fibrogenic response of hepatic stellate cells in vivo and in vitro by activating AMP-activated protein kinase

    Journal: World Journal of Gastroenterology

    doi: 10.3748/wjg.v24.i7.819

    Effect of metformin on VEGF expression and secretion of hepatic stellate cells and angiogenesis in vitro . A and B: HSCs were incubated with or without PDGF-BB (10 ng/mL) for 24 h or CoCl 2 (150 μmol/L) for 12 h and metformin (1, 2, 5, and 10 mmol/L). The expression levels of HIF-1α and VEGF were measured by Western blot analysis, and the results were quantified; C: Cells were treated as in panel B, and the supernatant was collected. The protein level of VEGF was measured by ELISA assay; D and E: HSCs were pretreated with metformin (5 and 10 mmol/L) or AICAR (500 μmol/L) for 2 h, and then incubated with or without CoCl 2 (150 μmol/L) for 12 h. The supernatant was collected and diluted 4:1 (v/v) in DMEM with 10% FBS to form conditioned medium. HUVECs were harvested and suspended in the conditioned medium, and then seeded on Matrigel. Images were acquired at 8 h (100 × magnification), and tube lengths were calculated with ImageJ and quantified. a P
    Figure Legend Snippet: Effect of metformin on VEGF expression and secretion of hepatic stellate cells and angiogenesis in vitro . A and B: HSCs were incubated with or without PDGF-BB (10 ng/mL) for 24 h or CoCl 2 (150 μmol/L) for 12 h and metformin (1, 2, 5, and 10 mmol/L). The expression levels of HIF-1α and VEGF were measured by Western blot analysis, and the results were quantified; C: Cells were treated as in panel B, and the supernatant was collected. The protein level of VEGF was measured by ELISA assay; D and E: HSCs were pretreated with metformin (5 and 10 mmol/L) or AICAR (500 μmol/L) for 2 h, and then incubated with or without CoCl 2 (150 μmol/L) for 12 h. The supernatant was collected and diluted 4:1 (v/v) in DMEM with 10% FBS to form conditioned medium. HUVECs were harvested and suspended in the conditioned medium, and then seeded on Matrigel. Images were acquired at 8 h (100 × magnification), and tube lengths were calculated with ImageJ and quantified. a P

    Techniques Used: Expressing, In Vitro, Incubation, Western Blot, Enzyme-linked Immunosorbent Assay

    10) Product Images from "Melatonin attenuates detrimental effects of diabetes on the niche of mouse spermatogonial stem cells by maintaining Leydig cells"

    Article Title: Melatonin attenuates detrimental effects of diabetes on the niche of mouse spermatogonial stem cells by maintaining Leydig cells

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-018-0956-4

    ERS suppresses the secretion of CSF1 in Leydig cell line. a CSF1 expression with Hoechst 33342 and their merges of MLTC-1 under three different ERS states (C control, Tm Tm treatment induced excessive ERS, Tm + 4PBA Tm treatment in combination with 4PBA for alleviated ERS). b CSF1 concentration in culture medium of MLTC-1 under the three different treatments was detected using ELISA. c RT-qPCR detected the mRNA expression level of Csf1 in MLTC-1 under the three treatments. d Expression of CSF1 in MLTC-1 under different treatments was measured by Western blot. Histograms are the statistical result of Image J (V1.48d) gradation analysis for the western blot experiments. e A graphical conclusion of this study is displayed: DM-induced high glucose activated ERS response factors (Grp78 and CHOP) in Leydig cells, resulting in apoptosis of Leydig cells and growth arrest of SSCs in testes. In response to these changes, melatonin treatment alleviated the apoptosis of Leydig cells via inhibition of ERS and recovered the CSF1 secretion in testes. CSF1 then resumed the self-renewal capacity of SSCs. (The results are expressed as the mean ± S.E.M of three separated wells of cells ( n = 3) in at least three different experiments and the statistical significance is expressed as follows: * p
    Figure Legend Snippet: ERS suppresses the secretion of CSF1 in Leydig cell line. a CSF1 expression with Hoechst 33342 and their merges of MLTC-1 under three different ERS states (C control, Tm Tm treatment induced excessive ERS, Tm + 4PBA Tm treatment in combination with 4PBA for alleviated ERS). b CSF1 concentration in culture medium of MLTC-1 under the three different treatments was detected using ELISA. c RT-qPCR detected the mRNA expression level of Csf1 in MLTC-1 under the three treatments. d Expression of CSF1 in MLTC-1 under different treatments was measured by Western blot. Histograms are the statistical result of Image J (V1.48d) gradation analysis for the western blot experiments. e A graphical conclusion of this study is displayed: DM-induced high glucose activated ERS response factors (Grp78 and CHOP) in Leydig cells, resulting in apoptosis of Leydig cells and growth arrest of SSCs in testes. In response to these changes, melatonin treatment alleviated the apoptosis of Leydig cells via inhibition of ERS and recovered the CSF1 secretion in testes. CSF1 then resumed the self-renewal capacity of SSCs. (The results are expressed as the mean ± S.E.M of three separated wells of cells ( n = 3) in at least three different experiments and the statistical significance is expressed as follows: * p

    Techniques Used: Expressing, Concentration Assay, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Western Blot, Inhibition

    Diabetes suppressed CSF1 expression in testes recovered by melatonin. a CSF1 expression with Hoechst 33342 and their merges of testicular sections from mice under four different treatments in the short term (W2, 2 weeks) and long term (W8, 8 weeks) experiments. Scale bar, 200 μm. b ELISA of CSF1 in mice serum of the four different groups in W2 and W8 experiments. c RT-qPCR detected Csf1 expression in mice testicular tissue under the four different treatments in W2 and W8 experiments. d CSF1 expression level detected by western blot analysis in the four groups in W2 and W8. Histograms are the statistical result of Image J (V1.48d) gradation analysis for the western blot experiments. (The results are shown as the mean ± S.E.M of at least three mice ( n = 3) and the statistical significance was expressed as follows: * p
    Figure Legend Snippet: Diabetes suppressed CSF1 expression in testes recovered by melatonin. a CSF1 expression with Hoechst 33342 and their merges of testicular sections from mice under four different treatments in the short term (W2, 2 weeks) and long term (W8, 8 weeks) experiments. Scale bar, 200 μm. b ELISA of CSF1 in mice serum of the four different groups in W2 and W8 experiments. c RT-qPCR detected Csf1 expression in mice testicular tissue under the four different treatments in W2 and W8 experiments. d CSF1 expression level detected by western blot analysis in the four groups in W2 and W8. Histograms are the statistical result of Image J (V1.48d) gradation analysis for the western blot experiments. (The results are shown as the mean ± S.E.M of at least three mice ( n = 3) and the statistical significance was expressed as follows: * p

    Techniques Used: Expressing, Mouse Assay, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Western Blot

    11) Product Images from "Metformin attenuates motility, contraction, and fibrogenic response of hepatic stellate cells in vivo and in vitro by activating AMP-activated protein kinase"

    Article Title: Metformin attenuates motility, contraction, and fibrogenic response of hepatic stellate cells in vivo and in vitro by activating AMP-activated protein kinase

    Journal: World Journal of Gastroenterology

    doi: 10.3748/wjg.v24.i7.819

    Effect of metformin on VEGF expression and secretion of hepatic stellate cells and angiogenesis in vitro . A and B: HSCs were incubated with or without PDGF-BB (10 ng/mL) for 24 h or CoCl 2 (150 μmol/L) for 12 h and metformin (1, 2, 5, and 10 mmol/L). The expression levels of HIF-1α and VEGF were measured by Western blot analysis, and the results were quantified; C: Cells were treated as in panel B, and the supernatant was collected. The protein level of VEGF was measured by ELISA assay; D and E: HSCs were pretreated with metformin (5 and 10 mmol/L) or AICAR (500 μmol/L) for 2 h, and then incubated with or without CoCl 2 (150 μmol/L) for 12 h. The supernatant was collected and diluted 4:1 (v/v) in DMEM with 10% FBS to form conditioned medium. HUVECs were harvested and suspended in the conditioned medium, and then seeded on Matrigel. Images were acquired at 8 h (100 × magnification), and tube lengths were calculated with ImageJ and quantified. a P
    Figure Legend Snippet: Effect of metformin on VEGF expression and secretion of hepatic stellate cells and angiogenesis in vitro . A and B: HSCs were incubated with or without PDGF-BB (10 ng/mL) for 24 h or CoCl 2 (150 μmol/L) for 12 h and metformin (1, 2, 5, and 10 mmol/L). The expression levels of HIF-1α and VEGF were measured by Western blot analysis, and the results were quantified; C: Cells were treated as in panel B, and the supernatant was collected. The protein level of VEGF was measured by ELISA assay; D and E: HSCs were pretreated with metformin (5 and 10 mmol/L) or AICAR (500 μmol/L) for 2 h, and then incubated with or without CoCl 2 (150 μmol/L) for 12 h. The supernatant was collected and diluted 4:1 (v/v) in DMEM with 10% FBS to form conditioned medium. HUVECs were harvested and suspended in the conditioned medium, and then seeded on Matrigel. Images were acquired at 8 h (100 × magnification), and tube lengths were calculated with ImageJ and quantified. a P

    Techniques Used: Expressing, In Vitro, Incubation, Western Blot, Enzyme-linked Immunosorbent Assay

    12) Product Images from "Separation of cell survival, growth, migration, and mesenchymal transdifferentiation effects of fibroblast secretome on tumor cells of head and neck squamous cell carcinoma"

    Article Title: Separation of cell survival, growth, migration, and mesenchymal transdifferentiation effects of fibroblast secretome on tumor cells of head and neck squamous cell carcinoma

    Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine

    doi: 10.1177/1010428317705507

    FIB and SCC-25 cells produce TGF-β1 and the effects of TGF-β1 on SCC-25 cell proliferation and migration. (a) The TGF-β1 concentrations in the supernatants were measured using ELISA after 3 days of treatment. SCC-25 cells treated with 5 ng/mL TGF-β1 contained 917.1 ± 38.12 pg/mL in the supernatant. In the supernatant of the albumin-medium-treated (control) SCC-25 cells, there was almost no detectable TGF-β1 (0.3 ± 0.12 pg/mL). Significant levels of TGF-β1 were measured in the supernatants of FIB CM (164.1 ± 6.85 pg/mL) and mixed-culture CM (106.0 ± 5.82 pg/mL)-treated SCC-25 cells, whereas the TGF-β1 levels in co-culture (2.3 ± 0.94 pg/mL) were low. In the supernatant of SCC-25-CM-treated cells 10.4 ± 2.53 pg/mL TGF-β1 was measured. (b) After treatment with 5 ng/mL TGF-β1, there were significantly (p
    Figure Legend Snippet: FIB and SCC-25 cells produce TGF-β1 and the effects of TGF-β1 on SCC-25 cell proliferation and migration. (a) The TGF-β1 concentrations in the supernatants were measured using ELISA after 3 days of treatment. SCC-25 cells treated with 5 ng/mL TGF-β1 contained 917.1 ± 38.12 pg/mL in the supernatant. In the supernatant of the albumin-medium-treated (control) SCC-25 cells, there was almost no detectable TGF-β1 (0.3 ± 0.12 pg/mL). Significant levels of TGF-β1 were measured in the supernatants of FIB CM (164.1 ± 6.85 pg/mL) and mixed-culture CM (106.0 ± 5.82 pg/mL)-treated SCC-25 cells, whereas the TGF-β1 levels in co-culture (2.3 ± 0.94 pg/mL) were low. In the supernatant of SCC-25-CM-treated cells 10.4 ± 2.53 pg/mL TGF-β1 was measured. (b) After treatment with 5 ng/mL TGF-β1, there were significantly (p

    Techniques Used: Migration, Enzyme-linked Immunosorbent Assay, Co-Culture Assay

    13) Product Images from "The long-term fate of mesenchymal stem cells labeled with magnetic resonance imaging-visible polymersomes in cerebral ischemia"

    Article Title: The long-term fate of mesenchymal stem cells labeled with magnetic resonance imaging-visible polymersomes in cerebral ischemia

    Journal: International Journal of Nanomedicine

    doi: 10.2147/IJN.S146742

    ELISA of grafted MSCs. Notes: Graphs show the concentration levels of BDNF ( A ), GDNF ( B ), VEGF ( C ), and IL-6 ( D ) in animals grafted with polymersome-labeled GFP-MSCs, unlabeled GFP-MSCs, and PBS. * p
    Figure Legend Snippet: ELISA of grafted MSCs. Notes: Graphs show the concentration levels of BDNF ( A ), GDNF ( B ), VEGF ( C ), and IL-6 ( D ) in animals grafted with polymersome-labeled GFP-MSCs, unlabeled GFP-MSCs, and PBS. * p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Concentration Assay, Labeling

    14) Product Images from "Inhibition of PTEN Ameliorates Secondary Hippocampal Injury and Cognitive Deficits after Intracerebral Hemorrhage: Involvement of AKT/FoxO3a/ATG-Mediated Autophagy"

    Article Title: Inhibition of PTEN Ameliorates Secondary Hippocampal Injury and Cognitive Deficits after Intracerebral Hemorrhage: Involvement of AKT/FoxO3a/ATG-Mediated Autophagy

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2021/5472605

    PTEN knockdown prevented hemorrhagic outcomes via suppressing neuronal autophagy. (a) Representative images of H E and Nissl staining in the hippocampal CA1 region at 3 d post-ICH. Bar, 50 μ m. (b) ELISA analysis of inflammatory cytokines TNF- α , IL-1 β , and IL-6 in the damaged hippocampus. (c–e) The effects of CQ on hippocampus-dependent learning and memory were assessed in the MWM test, Y-maze test, and PAT test. (f) Representative bands and quantitative analysis of LC3, Beclin-1, and p62 in the ipsilateral hippocampus post-ICH. ∗ P
    Figure Legend Snippet: PTEN knockdown prevented hemorrhagic outcomes via suppressing neuronal autophagy. (a) Representative images of H E and Nissl staining in the hippocampal CA1 region at 3 d post-ICH. Bar, 50 μ m. (b) ELISA analysis of inflammatory cytokines TNF- α , IL-1 β , and IL-6 in the damaged hippocampus. (c–e) The effects of CQ on hippocampus-dependent learning and memory were assessed in the MWM test, Y-maze test, and PAT test. (f) Representative bands and quantitative analysis of LC3, Beclin-1, and p62 in the ipsilateral hippocampus post-ICH. ∗ P

    Techniques Used: Staining, Enzyme-linked Immunosorbent Assay

    PTEN knockdown attenuated ICH-induced secondary hippocampal injury. (a–e) Representative images of H E staining (a, b, c), Nissl staining (d), and caspase-3 IHC staining (e) in the hippocampal CA1 region at 3 d after ICH in rats. Images in (a) and (b) showed the site of brain hemorrhage and the CA1 region of the hippocampus, respectively. Bar, 50 μ m. (f) The quantitative analysis of caspase-3 protein normalized to the control group. (g) The impacts of PTEN inhibition on hippocampal neuroinflammation by analyzing the contents of TNF- α , IL-1 β , and IL-6 in the ipsilateral hippocampus using ELISA analysis at 3 d postinjury. ∗ P
    Figure Legend Snippet: PTEN knockdown attenuated ICH-induced secondary hippocampal injury. (a–e) Representative images of H E staining (a, b, c), Nissl staining (d), and caspase-3 IHC staining (e) in the hippocampal CA1 region at 3 d after ICH in rats. Images in (a) and (b) showed the site of brain hemorrhage and the CA1 region of the hippocampus, respectively. Bar, 50 μ m. (f) The quantitative analysis of caspase-3 protein normalized to the control group. (g) The impacts of PTEN inhibition on hippocampal neuroinflammation by analyzing the contents of TNF- α , IL-1 β , and IL-6 in the ipsilateral hippocampus using ELISA analysis at 3 d postinjury. ∗ P

    Techniques Used: Staining, Immunohistochemistry, Inhibition, Enzyme-linked Immunosorbent Assay

    15) Product Images from "GHK Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice by Suppressing TGFβ1/Smad-Mediated Epithelial-to-Mesenchymal Transition"

    Article Title: GHK Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice by Suppressing TGFβ1/Smad-Mediated Epithelial-to-Mesenchymal Transition

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2017.00904

    Effects of GHK on TGF-β1 mRNA and protein expression in mice with BLM-induced fibrosis. (A) TGF-β1 expression levels in lung tissues in each group were determined by real-time PCR. (B) TGF-β1 activity in lung tissues was measured by an ELISA kit. (C) TGF-β1 protein expression in lung tissues in each group was measured by western blot analysis. (D) The densitometry values of the proteins were normalized to those of β-actin. All data represent the mean ± SEM of three independent experiments performed in triplicate. Statistical analysis was performed by one-way ANOVA and Turkey’s multiple-comparison test; compared with control group, ## P
    Figure Legend Snippet: Effects of GHK on TGF-β1 mRNA and protein expression in mice with BLM-induced fibrosis. (A) TGF-β1 expression levels in lung tissues in each group were determined by real-time PCR. (B) TGF-β1 activity in lung tissues was measured by an ELISA kit. (C) TGF-β1 protein expression in lung tissues in each group was measured by western blot analysis. (D) The densitometry values of the proteins were normalized to those of β-actin. All data represent the mean ± SEM of three independent experiments performed in triplicate. Statistical analysis was performed by one-way ANOVA and Turkey’s multiple-comparison test; compared with control group, ## P

    Techniques Used: Expressing, Mouse Assay, Real-time Polymerase Chain Reaction, Activity Assay, Enzyme-linked Immunosorbent Assay, Western Blot

    Effects of GHK on lung histological changes in mice with BLM-induced fibrosis. (A) BLM administration caused significant body weight loss, while GHK treatment attenuated body weight loss. (B) The lung W/D weight ratio was calculated using some left lobes. BLM administration increased the W/D weight ratio, whereas GHK reversed the change caused by BLM administration. (C) MPO activity levels in lung extracts. BLM administration increased MPO activity in the lung extracts, while GHK treatment normalized MPO activity in the lung extracts. (D) Chronic inflammation was significantly induced by intratracheal BLM administration, while GHK treatment reduced BLM-induced chronic inflammation. (E) Lung sections were stained with HE for histological assessment, and representative images are shown. (F) TNF-α levels in BALF were evaluated by ELISA kits. (G) IL-6 levels in BALF were evaluated by ELISA kits. The bars represent the mean ± SEM; statistical analysis was performed by one-way ANOVA and Turkey’s multiple-comparison test; compared with control group, ## P
    Figure Legend Snippet: Effects of GHK on lung histological changes in mice with BLM-induced fibrosis. (A) BLM administration caused significant body weight loss, while GHK treatment attenuated body weight loss. (B) The lung W/D weight ratio was calculated using some left lobes. BLM administration increased the W/D weight ratio, whereas GHK reversed the change caused by BLM administration. (C) MPO activity levels in lung extracts. BLM administration increased MPO activity in the lung extracts, while GHK treatment normalized MPO activity in the lung extracts. (D) Chronic inflammation was significantly induced by intratracheal BLM administration, while GHK treatment reduced BLM-induced chronic inflammation. (E) Lung sections were stained with HE for histological assessment, and representative images are shown. (F) TNF-α levels in BALF were evaluated by ELISA kits. (G) IL-6 levels in BALF were evaluated by ELISA kits. The bars represent the mean ± SEM; statistical analysis was performed by one-way ANOVA and Turkey’s multiple-comparison test; compared with control group, ## P

    Techniques Used: Mouse Assay, Activity Assay, Staining, Enzyme-linked Immunosorbent Assay

    16) Product Images from "Effects of Cordycepin on the Microglia-Overactivation-Induced Impairments of Growth and Development of Hippocampal Cultured Neurons"

    Article Title: Effects of Cordycepin on the Microglia-Overactivation-Induced Impairments of Growth and Development of Hippocampal Cultured Neurons

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0125902

    Cordycepin attenuated the LPS-induced inflammatory responses. (A) Representative images of microglia following 10 μM cordycepin treatment for 1 day with or without LPS treatment. Cells were stained green for tubulin, blue for nucleus. Scale bar = 100μm. The contents of cytokines, including TNF-α (B) and IL-1β (C) in the experimental groups were measured by the ELISA assay. Note the obviously lower concentrations of TNF-α and IL-1β in cordycepin treatment group compared to untreated group after LPS stimulation. (D-E) Relative mRNA levels of iNOS and COX-2 in the experimental groups assessed by real time PCR using the 2 -ΔΔCT method. Data are expressed as the fold change in gene expression normalized to an endogenous gene (β-actin) and relative to the cells in control group without LPS stimulation. Data are presented as mean ± SEM (n = 6 in triplicate). # p
    Figure Legend Snippet: Cordycepin attenuated the LPS-induced inflammatory responses. (A) Representative images of microglia following 10 μM cordycepin treatment for 1 day with or without LPS treatment. Cells were stained green for tubulin, blue for nucleus. Scale bar = 100μm. The contents of cytokines, including TNF-α (B) and IL-1β (C) in the experimental groups were measured by the ELISA assay. Note the obviously lower concentrations of TNF-α and IL-1β in cordycepin treatment group compared to untreated group after LPS stimulation. (D-E) Relative mRNA levels of iNOS and COX-2 in the experimental groups assessed by real time PCR using the 2 -ΔΔCT method. Data are expressed as the fold change in gene expression normalized to an endogenous gene (β-actin) and relative to the cells in control group without LPS stimulation. Data are presented as mean ± SEM (n = 6 in triplicate). # p

    Techniques Used: Staining, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, Expressing

    17) Product Images from "Wogonin, a plant derived small molecule, exerts potent anti-inflammatory and chondroprotective effects through the activation of ROS/ERK/Nrf2 signaling pathways in human Osteoarthritis chondrocytes"

    Article Title: Wogonin, a plant derived small molecule, exerts potent anti-inflammatory and chondroprotective effects through the activation of ROS/ERK/Nrf2 signaling pathways in human Osteoarthritis chondrocytes

    Journal: Free radical biology & medicine

    doi: 10.1016/j.freeradbiomed.2017.02.041

    Wogonin (WG) inhibited the IL-1β induced matrix degradation in human OA chondrocytes and cartilage explants Human OA chondrocytes were pre-treated with Wogonin (10–50 μM) for 2 h followed by treatment with IL-1β (1 ng/ml) for 16 h. At the end of treatment culture supernatant were collected and chondrocytes were harvested. Cell lysate were prepared using RIPA buffer for immunoblot analysis or RNA were isolated for real time PCR analysis. (A) Expression of MMP-3, MMP-9, MMP-13 and ADAMTS-4 was measured by quantitative PCR using the TaqMan assay system (Life Technologies). β-actin was used as endogenous expression control. (B) Protein expression of secreted MMP-13, MMP-3, cytosolic MMP-13, MMP-9, MMP-3, ADAMTS-4 and COL2A1 was investigated by immunoblotting using antibodies against indicated protein. β-actin was used as a control for equal loading. Specific signal intensities were quantified by ImageJ software. (C) Secreted level of MMP-13 production was measured in the culture supernatant using ELISA. The data was expressed relative to untreated controls. (D) Collagenase/gelatinase activity in the culture supernatant was measured using method described in method section. Supernatant were collected from OA chondrocytes (1×10 6 /well of 12-well plate in 0.5 ml) treated with Wogonin (10–50 μM) for 2 h and then stimulated with IL-1β (25 ng/ml) for 16 h. Activity was expressed relative to untreated controls. (E) MMP-13 activity in the culture media activated using APMA (1 mM, 40 minutes) was determined by fluorogenic peptide assay using commercially available kit (AnaSpec). Supernatant were collected from OA chondrocytes (1×10 6 /well of 6-well plate) treated with Wogonin (10–50 μM) for 2 h and then stimulated with IL-1β (25 ng/ml) for 16 h. Activity was expressed relative to untreated controls. (F) Expression of COL2A1 and ACAN was measured by quantitative PCR using the TaqMan assay system (Life Technologies). β-actin was used as endogenous expression control. (G) The release of COL2A1 levels, (H) COL2A1 content in cartilage explants and (I) release of s-GAG levels was estimated in supernatants isolated from culture of OA cartilage explants treated with Wogonin (10–50 μM) for 2 h followed by treatment with IL-1β (25 ng/ml) for 72 h. (J) Histopathological section of cartilage explants treated with Wogonin (10–50 μM) for 2 h followed by treatment with IL-1β (25 ng/ml) for 72 h, fixed in 4% PFA and embedded in paraffin. Explant sections (6 μm) were stained with Safranin O and fast green and imaged using Nikon eclipse Ti inverted microscope. The scale bar is shown as 100 μm. Bar graph represents mean±SD from three subjects. Immunoblot results are representatives of two blots performed on samples obtained from two individuals *p≤0.01, as compared to control, #≤0.01, as compared to IL-1β.
    Figure Legend Snippet: Wogonin (WG) inhibited the IL-1β induced matrix degradation in human OA chondrocytes and cartilage explants Human OA chondrocytes were pre-treated with Wogonin (10–50 μM) for 2 h followed by treatment with IL-1β (1 ng/ml) for 16 h. At the end of treatment culture supernatant were collected and chondrocytes were harvested. Cell lysate were prepared using RIPA buffer for immunoblot analysis or RNA were isolated for real time PCR analysis. (A) Expression of MMP-3, MMP-9, MMP-13 and ADAMTS-4 was measured by quantitative PCR using the TaqMan assay system (Life Technologies). β-actin was used as endogenous expression control. (B) Protein expression of secreted MMP-13, MMP-3, cytosolic MMP-13, MMP-9, MMP-3, ADAMTS-4 and COL2A1 was investigated by immunoblotting using antibodies against indicated protein. β-actin was used as a control for equal loading. Specific signal intensities were quantified by ImageJ software. (C) Secreted level of MMP-13 production was measured in the culture supernatant using ELISA. The data was expressed relative to untreated controls. (D) Collagenase/gelatinase activity in the culture supernatant was measured using method described in method section. Supernatant were collected from OA chondrocytes (1×10 6 /well of 12-well plate in 0.5 ml) treated with Wogonin (10–50 μM) for 2 h and then stimulated with IL-1β (25 ng/ml) for 16 h. Activity was expressed relative to untreated controls. (E) MMP-13 activity in the culture media activated using APMA (1 mM, 40 minutes) was determined by fluorogenic peptide assay using commercially available kit (AnaSpec). Supernatant were collected from OA chondrocytes (1×10 6 /well of 6-well plate) treated with Wogonin (10–50 μM) for 2 h and then stimulated with IL-1β (25 ng/ml) for 16 h. Activity was expressed relative to untreated controls. (F) Expression of COL2A1 and ACAN was measured by quantitative PCR using the TaqMan assay system (Life Technologies). β-actin was used as endogenous expression control. (G) The release of COL2A1 levels, (H) COL2A1 content in cartilage explants and (I) release of s-GAG levels was estimated in supernatants isolated from culture of OA cartilage explants treated with Wogonin (10–50 μM) for 2 h followed by treatment with IL-1β (25 ng/ml) for 72 h. (J) Histopathological section of cartilage explants treated with Wogonin (10–50 μM) for 2 h followed by treatment with IL-1β (25 ng/ml) for 72 h, fixed in 4% PFA and embedded in paraffin. Explant sections (6 μm) were stained with Safranin O and fast green and imaged using Nikon eclipse Ti inverted microscope. The scale bar is shown as 100 μm. Bar graph represents mean±SD from three subjects. Immunoblot results are representatives of two blots performed on samples obtained from two individuals *p≤0.01, as compared to control, #≤0.01, as compared to IL-1β.

    Techniques Used: Isolation, Real-time Polymerase Chain Reaction, Expressing, TaqMan Assay, Software, Enzyme-linked Immunosorbent Assay, Activity Assay, Staining, Inverted Microscopy

    Wogonin (WG) inhibited the IL1-β induced inflammatory mediators in human OA chondrocytes Primary human OA chondrocytes were pre-treated with Wogonin (10–50 μM) for 2 h followed by treatment with IL-1β (1 ng/ml) for 16 h. At the end of treatment culture supernatant were collected and chondrocytes were harvested. Cell lysate were prepared using RIPA buffer for immunoblot analysis or RNA were isolated for real time PCR analysis. (A) Expression of IL-6, COX-2 and iNOS was measured by quantitative PCR using the TaqMan assay system (Life Technologies). β-actin was used as endogenous expression control. (B) Protein expression of secreted IL-6, cytosolic IL-6, COX-2 and iNOS was investigated by immunoblotting using antibodies against indicated protein. β-actin was used as a control for equal loading. Specific signal intensities were quantified by ImageJ software. (C–D) Secreted levels of IL-6 (C) and PGE2 production (D) were measured in the culture supernatant by ELISA (E) Production of NO was estimated in supernatant using Griess assay as described in methods. Bar graph represents mean±SD from two subjects. *p≤0.01, as compared to control, #≤0.01, as compared to IL-1β.
    Figure Legend Snippet: Wogonin (WG) inhibited the IL1-β induced inflammatory mediators in human OA chondrocytes Primary human OA chondrocytes were pre-treated with Wogonin (10–50 μM) for 2 h followed by treatment with IL-1β (1 ng/ml) for 16 h. At the end of treatment culture supernatant were collected and chondrocytes were harvested. Cell lysate were prepared using RIPA buffer for immunoblot analysis or RNA were isolated for real time PCR analysis. (A) Expression of IL-6, COX-2 and iNOS was measured by quantitative PCR using the TaqMan assay system (Life Technologies). β-actin was used as endogenous expression control. (B) Protein expression of secreted IL-6, cytosolic IL-6, COX-2 and iNOS was investigated by immunoblotting using antibodies against indicated protein. β-actin was used as a control for equal loading. Specific signal intensities were quantified by ImageJ software. (C–D) Secreted levels of IL-6 (C) and PGE2 production (D) were measured in the culture supernatant by ELISA (E) Production of NO was estimated in supernatant using Griess assay as described in methods. Bar graph represents mean±SD from two subjects. *p≤0.01, as compared to control, #≤0.01, as compared to IL-1β.

    Techniques Used: Isolation, Real-time Polymerase Chain Reaction, Expressing, TaqMan Assay, Software, Enzyme-linked Immunosorbent Assay, Griess Assay

    18) Product Images from "Proteomic Screening of Anaerobically Regulated Promoters from Salmonella and Its Antitumor Applications *"

    Article Title: Proteomic Screening of Anaerobically Regulated Promoters from Salmonella and Its Antitumor Applications *

    Journal: Molecular & Cellular Proteomics : MCP

    doi: 10.1074/mcp.M111.009399

    VNP padhEEndostatin inhibited neoangiogenesis in vitro and in vivo . A , CAM assay. Variable amount of bacteria was applied to the CAMs of 8-day-old chick embryos. After 48 h, the avascular zone (≈1 cm in diameter) of each CAM was observed. The representative appearance of chick CAMs implanted with a coverslip containing VNP padhEEndostatin (200 μg/embryo or 100 μg/embryo), VNP with empty vector (200 μg/embryo) or PBS are shown. The marked square indicates the location of the implanted filter disk. An avascular zone around the filter disk was observed only with VNP padhEEndostatin treatment. B , VEGF expression following VNP padhEEndostatin therapy. Tumors were dissected 12 days post-treatment. Tumor weights were measured and VEGF levels in tumor extracts were determined by ELISA. (Mean ± S.D., n = 3, * p
    Figure Legend Snippet: VNP padhEEndostatin inhibited neoangiogenesis in vitro and in vivo . A , CAM assay. Variable amount of bacteria was applied to the CAMs of 8-day-old chick embryos. After 48 h, the avascular zone (≈1 cm in diameter) of each CAM was observed. The representative appearance of chick CAMs implanted with a coverslip containing VNP padhEEndostatin (200 μg/embryo or 100 μg/embryo), VNP with empty vector (200 μg/embryo) or PBS are shown. The marked square indicates the location of the implanted filter disk. An avascular zone around the filter disk was observed only with VNP padhEEndostatin treatment. B , VEGF expression following VNP padhEEndostatin therapy. Tumors were dissected 12 days post-treatment. Tumor weights were measured and VEGF levels in tumor extracts were determined by ELISA. (Mean ± S.D., n = 3, * p

    Techniques Used: In Vitro, In Vivo, Chick Chorioallantoic Membrane Assay, Plasmid Preparation, Expressing, Enzyme-linked Immunosorbent Assay

    19) Product Images from "Molecular Pathways Associated with Kallikrein 6 Overexpression in Colorectal Cancer"

    Article Title: Molecular Pathways Associated with Kallikrein 6 Overexpression in Colorectal Cancer

    Journal: Genes

    doi: 10.3390/genes12050749

    Evaluation of the transcript levels of selected co-expressed genes and KLK6 secretion in the CRC patient-derived organoid cultures. ( A ) KRT6A, KRT6B and c-MYC transcript levels. ( B ) KLK6, FOSL1 , and HMGA2 transcript levels. ( C ) Levels of secreted KLK6 in the conditioned media of the tumor organoid cultures by ELISA.
    Figure Legend Snippet: Evaluation of the transcript levels of selected co-expressed genes and KLK6 secretion in the CRC patient-derived organoid cultures. ( A ) KRT6A, KRT6B and c-MYC transcript levels. ( B ) KLK6, FOSL1 , and HMGA2 transcript levels. ( C ) Levels of secreted KLK6 in the conditioned media of the tumor organoid cultures by ELISA.

    Techniques Used: Derivative Assay, Enzyme-linked Immunosorbent Assay

    20) Product Images from "β2-Adrenergic Receptor-Mediated HIF-1α Upregulation Mediates Blood Brain Barrier Damage in Acute Cerebral Ischemia"

    Article Title: β2-Adrenergic Receptor-Mediated HIF-1α Upregulation Mediates Blood Brain Barrier Damage in Acute Cerebral Ischemia

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2017.00257

    Effect of HIF-1α inhibition by YC-1 or HIF-1α siRNA on 2-h oxygen glucose deprivation (OGD)-induced VEGF secretion in neurons. The neurons were exposed to OGD for 2 h and VEGF secretion was assessed by measuring its content in cellular extracts (CE) and conditioned media (CM) using western blot and ELISA respectively. Two-hours OGD induced a significant increase in VEGF mRNA expression in neurons and pretreatment with YC-1 ( A , left panel) or HIF-1α siR ( A , right panel) significantly inhibited this effect. ** P
    Figure Legend Snippet: Effect of HIF-1α inhibition by YC-1 or HIF-1α siRNA on 2-h oxygen glucose deprivation (OGD)-induced VEGF secretion in neurons. The neurons were exposed to OGD for 2 h and VEGF secretion was assessed by measuring its content in cellular extracts (CE) and conditioned media (CM) using western blot and ELISA respectively. Two-hours OGD induced a significant increase in VEGF mRNA expression in neurons and pretreatment with YC-1 ( A , left panel) or HIF-1α siR ( A , right panel) significantly inhibited this effect. ** P

    Techniques Used: Inhibition, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing

    21) Product Images from "Investigation of Association of Complement 5 Genetic Polymorphisms with Sepsis and Sepsis-Induced Inflammatory Responses"

    Article Title: Investigation of Association of Complement 5 Genetic Polymorphisms with Sepsis and Sepsis-Induced Inflammatory Responses

    Journal: Journal of Inflammation Research

    doi: 10.2147/JIR.S340446

    C5a enhances LPS-induced inflammatory cytokine production and cell apoptosis. THP-1 monocytes were stimulated with C5a (100 ng/mL), LPS (500 ng/mL), or C5a plus LPS for 16 h in vitro. ( A – C ) The supernatant concentrations of inflammatory cytokines (IL-1β, TNF-α and IL-6) were measured by ELISA; ( D and E ) the apoptosis of THP-1 monocytes stimulated with C5a, LPS, or C5a plus LPS was also measured by using annexin-V-FITC/PI staining on a flow cytometer. Values of relative expression levels are shown as mean ± SD; * P
    Figure Legend Snippet: C5a enhances LPS-induced inflammatory cytokine production and cell apoptosis. THP-1 monocytes were stimulated with C5a (100 ng/mL), LPS (500 ng/mL), or C5a plus LPS for 16 h in vitro. ( A – C ) The supernatant concentrations of inflammatory cytokines (IL-1β, TNF-α and IL-6) were measured by ELISA; ( D and E ) the apoptosis of THP-1 monocytes stimulated with C5a, LPS, or C5a plus LPS was also measured by using annexin-V-FITC/PI staining on a flow cytometer. Values of relative expression levels are shown as mean ± SD; * P

    Techniques Used: In Vitro, Enzyme-linked Immunosorbent Assay, Staining, Flow Cytometry, Expressing

    22) Product Images from "Loss of the androgen receptor suppresses intrarenal calcium oxalate crystals deposition via altering macrophage recruitment/M2 polarization with change of the miR-185-5p/CSF-1 signals"

    Article Title: Loss of the androgen receptor suppresses intrarenal calcium oxalate crystals deposition via altering macrophage recruitment/M2 polarization with change of the miR-185-5p/CSF-1 signals

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-019-1358-y

    Loss of androgen receptor (AR) increased renal CSF-1 expression and M2 macrophage infiltration in glyoxylate-induced intrarenal calcium oxalate (CaOx) crystals deposition mouse model. a The quantitative real-time PCR (qRT-PCR) analysis of CSF-1 gene and miR-185-5p expression in mice kidneys. b (IHC staining of mouse kidney tissues showing that loss of AR in Cdh16-ARKO mice increased the CSF-1 expression. Quantification of CSF-1 positive renal tubules is shown in the right panel. c Kidney CSF-1 levels in WT and Cdh16-ARKO mice. CSF-1 levels in kidney homogenates determined by ELISA. d Representative MISH staining results for mmu-miR-185-5p in kidney tissues from WT or Cdh16-ARKO mice. e AR deletion in the renal tubule led to increased mRNA levels of markers of pan-MΦs and M2-like MΦs, including F4/80, CD163, CD206 (mannose receptor), but not INOS, in kidneys from mice with glyoxylate injection for 6 days. f Immunostaining indicated increased renal F4/80-positive MΦs in the renal corticomedullary junction from Cdh16-ARKO mice at 6 days after glyoxylate injection. g Immunostaining indicated increased renal CD163-positive MΦs in the renal corticomedullary junction from Cdh16-ARKO mice at 6 days after glyoxylate injection. h Immunofluorescence indicated increased renal CD206-positive MΦs in the Cdh16-ARKO mice at 6 days after glyoxylate injection. For B, D, F, G and H, quantitations are at the right and all quantitations are mean ± SD, * P
    Figure Legend Snippet: Loss of androgen receptor (AR) increased renal CSF-1 expression and M2 macrophage infiltration in glyoxylate-induced intrarenal calcium oxalate (CaOx) crystals deposition mouse model. a The quantitative real-time PCR (qRT-PCR) analysis of CSF-1 gene and miR-185-5p expression in mice kidneys. b (IHC staining of mouse kidney tissues showing that loss of AR in Cdh16-ARKO mice increased the CSF-1 expression. Quantification of CSF-1 positive renal tubules is shown in the right panel. c Kidney CSF-1 levels in WT and Cdh16-ARKO mice. CSF-1 levels in kidney homogenates determined by ELISA. d Representative MISH staining results for mmu-miR-185-5p in kidney tissues from WT or Cdh16-ARKO mice. e AR deletion in the renal tubule led to increased mRNA levels of markers of pan-MΦs and M2-like MΦs, including F4/80, CD163, CD206 (mannose receptor), but not INOS, in kidneys from mice with glyoxylate injection for 6 days. f Immunostaining indicated increased renal F4/80-positive MΦs in the renal corticomedullary junction from Cdh16-ARKO mice at 6 days after glyoxylate injection. g Immunostaining indicated increased renal CD163-positive MΦs in the renal corticomedullary junction from Cdh16-ARKO mice at 6 days after glyoxylate injection. h Immunofluorescence indicated increased renal CD206-positive MΦs in the Cdh16-ARKO mice at 6 days after glyoxylate injection. For B, D, F, G and H, quantitations are at the right and all quantitations are mean ± SD, * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Mouse Assay, Immunohistochemistry, Staining, Enzyme-linked Immunosorbent Assay, Injection, Immunostaining, Immunofluorescence

    Knocking down androgen receptor (AR) in renal tubular epithelial cells (RTCs) enhanced the macrophages migration and M2 polarization via modulating the CSF-1 signals. a-c Cells were pre-treated with shAR or with scrambled control (scr). After 72-h incubation, cells were treated with 20 μg/cm 2 COM crystals for 24 h. a Quantitative real-time PCR (qRT-PCR) analysis of MΦs-associated cytokines in HK-2 and HKC-8 cells with/without knockdown of AR. b The level of CSF-1 in the CM of RTCs was detected by ELISA. c The level of CSF-1 in the RTCs lysates was detected by western blot. d qRT-PCR (left panels) and western blot (right panels) show CSF-1 knockdown efficiency in HK-2 and HKC-8 cells. e Knocking down AR in HK-2 and HKC-8 cells increased M0-MΦs migration, whereas knocking down CSF-1 interrupted the AR knockdown-mediated increase of M0-MΦs migration. f CM from AR-depleted RTCs led to increase mRNA levels of markers of M2 phenotypic MΦs (CD163 and CD206), whereas knocking down CSF-1 in RTCs interrupted AR knockdown-mediated M2-MΦs markers change. g Flow cytometry analysis showed that CM from AR-depleted RTCs led to increase expressions markers of M2 phenotypic MΦs (CD163 and CD206), whereas knocking down CSF-1 in RTCs interrupted AR knockdown-mediated M2-MΦs markers change. h Knocking down CSF-1 in HK-2 and HKC-8 partly reversed the AR knockdown-enhanced COM crystals phagocytic ability of MΦs. For e, g and h , quantifications are at the right. All quantitations are presented as mean ± SD. * P
    Figure Legend Snippet: Knocking down androgen receptor (AR) in renal tubular epithelial cells (RTCs) enhanced the macrophages migration and M2 polarization via modulating the CSF-1 signals. a-c Cells were pre-treated with shAR or with scrambled control (scr). After 72-h incubation, cells were treated with 20 μg/cm 2 COM crystals for 24 h. a Quantitative real-time PCR (qRT-PCR) analysis of MΦs-associated cytokines in HK-2 and HKC-8 cells with/without knockdown of AR. b The level of CSF-1 in the CM of RTCs was detected by ELISA. c The level of CSF-1 in the RTCs lysates was detected by western blot. d qRT-PCR (left panels) and western blot (right panels) show CSF-1 knockdown efficiency in HK-2 and HKC-8 cells. e Knocking down AR in HK-2 and HKC-8 cells increased M0-MΦs migration, whereas knocking down CSF-1 interrupted the AR knockdown-mediated increase of M0-MΦs migration. f CM from AR-depleted RTCs led to increase mRNA levels of markers of M2 phenotypic MΦs (CD163 and CD206), whereas knocking down CSF-1 in RTCs interrupted AR knockdown-mediated M2-MΦs markers change. g Flow cytometry analysis showed that CM from AR-depleted RTCs led to increase expressions markers of M2 phenotypic MΦs (CD163 and CD206), whereas knocking down CSF-1 in RTCs interrupted AR knockdown-mediated M2-MΦs markers change. h Knocking down CSF-1 in HK-2 and HKC-8 partly reversed the AR knockdown-enhanced COM crystals phagocytic ability of MΦs. For e, g and h , quantifications are at the right. All quantitations are presented as mean ± SD. * P

    Techniques Used: Migration, Incubation, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Western Blot, Flow Cytometry, Cytometry

    Androgen receptor (AR) modulates CSF-1 via upregulation of miR-185-5p in renal tubular epithelial cells (RTCs) exposed to calcium oxalate monohydrate (COM) crystals. a Eighteen potential miRNAs candidates were screened by quantitative real-time PCR (qRT-PCR) assay in HK-2 cells and HKC-8 cells based on their response to knocking down AR. Cells were pre-treated with 20 μg/cm 2 COM crystals for 24 h. b The qRT-PCR analysis of five miRNAs in both HK-2 and HKC-8 cells with shAR compared with control. c, d HK-2 and HKC-8 cells were virally transduced with miR-15a-5p, miR-130b-3p, miR-185-5p, miR-650, and miR-1207-5p. Cells were then exposed to 20 μg/cm 2 COM crystals for 24 h. Total RNAs ( c ) were analyzed for CSF-1 by qRT-PCR. The protein expression levels ( d ) of CSF-1 in the CM of HK-2 and HKC-8 cells were assessed by ELISA. e The mRNA levels of CSF-1 were determined by qRT-PCR analysis after co-transfection with shAR and miR-185-5p (vs. scramble). f The protein levels of CSF-1 in RTCs CM were determined by ELISA after co-transfection with shAR and miR-185-5p (vs. scramble). g M0-MΦs migration to the CM from HK-2 cells (upper) and HKC-8 cells (lower) with four groups (scramble, shAR, miR-185-5p, and shAR + miR-185-5p). h Overexpressing miR-185-5p in HK-2 cells and HKC-8 cells partly reversed the AR knockdown-enhanced COM crystals phagocytic ability of MΦs. For g and h , quantifications are at the right. All quantitations are presented as mean ± SD. * P
    Figure Legend Snippet: Androgen receptor (AR) modulates CSF-1 via upregulation of miR-185-5p in renal tubular epithelial cells (RTCs) exposed to calcium oxalate monohydrate (COM) crystals. a Eighteen potential miRNAs candidates were screened by quantitative real-time PCR (qRT-PCR) assay in HK-2 cells and HKC-8 cells based on their response to knocking down AR. Cells were pre-treated with 20 μg/cm 2 COM crystals for 24 h. b The qRT-PCR analysis of five miRNAs in both HK-2 and HKC-8 cells with shAR compared with control. c, d HK-2 and HKC-8 cells were virally transduced with miR-15a-5p, miR-130b-3p, miR-185-5p, miR-650, and miR-1207-5p. Cells were then exposed to 20 μg/cm 2 COM crystals for 24 h. Total RNAs ( c ) were analyzed for CSF-1 by qRT-PCR. The protein expression levels ( d ) of CSF-1 in the CM of HK-2 and HKC-8 cells were assessed by ELISA. e The mRNA levels of CSF-1 were determined by qRT-PCR analysis after co-transfection with shAR and miR-185-5p (vs. scramble). f The protein levels of CSF-1 in RTCs CM were determined by ELISA after co-transfection with shAR and miR-185-5p (vs. scramble). g M0-MΦs migration to the CM from HK-2 cells (upper) and HKC-8 cells (lower) with four groups (scramble, shAR, miR-185-5p, and shAR + miR-185-5p). h Overexpressing miR-185-5p in HK-2 cells and HKC-8 cells partly reversed the AR knockdown-enhanced COM crystals phagocytic ability of MΦs. For g and h , quantifications are at the right. All quantitations are presented as mean ± SD. * P

    Techniques Used: Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Transduction, Expressing, Enzyme-linked Immunosorbent Assay, Cotransfection, Migration

    23) Product Images from "The Heparan Sulfate Proteoglycan Syndecan-1 Influences Local Bone Cell Communication via the RANKL/OPG Axis"

    Article Title: The Heparan Sulfate Proteoglycan Syndecan-1 Influences Local Bone Cell Communication via the RANKL/OPG Axis

    Journal: bioRxiv

    doi: 10.1101/852590

    Osteoclast differentiation and RANKL/OPG release in co-cultures of osteoblasts and osteoclasts using Syndecan-1 deficient cells. Primary osteoblast (2×10 4 cells/well) and osteoclast precursor cells (4×10 5 cells/well) were cultured together in DM+-medium (see Table 1 ) for up to 7 days. Different combinations of genotypes (WT/Sdc1-/-) as depicted were used (OB/OC). A: After 7 days, the osteoblast layer was removed and TRAP staining was performed, scale bar 200µm. Osteoclast number was determined as TRAP positive, multinucleated cells, Quantification in panel B. C: OPG and RANKL concentrations were determined in cell culture supernatant using ELISA. D: RANKL/OPG ratio was calculated. Experiments were performed in independent triplicates, data represent mean ± SD, 2way ANOVA with Bonferronís test, *p
    Figure Legend Snippet: Osteoclast differentiation and RANKL/OPG release in co-cultures of osteoblasts and osteoclasts using Syndecan-1 deficient cells. Primary osteoblast (2×10 4 cells/well) and osteoclast precursor cells (4×10 5 cells/well) were cultured together in DM+-medium (see Table 1 ) for up to 7 days. Different combinations of genotypes (WT/Sdc1-/-) as depicted were used (OB/OC). A: After 7 days, the osteoblast layer was removed and TRAP staining was performed, scale bar 200µm. Osteoclast number was determined as TRAP positive, multinucleated cells, Quantification in panel B. C: OPG and RANKL concentrations were determined in cell culture supernatant using ELISA. D: RANKL/OPG ratio was calculated. Experiments were performed in independent triplicates, data represent mean ± SD, 2way ANOVA with Bonferronís test, *p

    Techniques Used: Cell Culture, Staining, Enzyme-linked Immunosorbent Assay

    Syndecan-1 concentration in serum of mice increases with age. Serum of 4, 12 and 18 month old mice (wild type) was collected. Concentration of soluble Syndecan-1 was determined by ELISA. Data are displayed as mean ± SD, Kruskal-Wallis test with Dunńs post hoc test, n =9-13 per group. *p
    Figure Legend Snippet: Syndecan-1 concentration in serum of mice increases with age. Serum of 4, 12 and 18 month old mice (wild type) was collected. Concentration of soluble Syndecan-1 was determined by ELISA. Data are displayed as mean ± SD, Kruskal-Wallis test with Dunńs post hoc test, n =9-13 per group. *p

    Techniques Used: Concentration Assay, Mouse Assay, Enzyme-linked Immunosorbent Assay

    Expression of Syndecan-1 in osteoblasts and osteoclasts during differentiation in vitro.. Co-cultures of osteoblasts and osteoclasts were performed in presence of 1,25(OH) 2 D 3 and PGE2 (DM+, see Table 1 ). AB: mRNA expression of Syndecan-1-4 were analysed using quantitative realtime PCR (Primers see Table 2 ) normalized to HPRT and day 1 of culture (ΔΔCT method). C: Protein expression of Syndecan-1 in the cells was detected using a polyclonal antibody against Syndecan-1. Scale bar: 50µm. D: Syndecan-1 expression was analysed after stimulation of osteoblastic cells with DM+ medium. mRNA expression was determined by realtime PCR (left). The concentration of soluble Syndecan-1 protein in the supernatant of cells was analysed by ELISA (right). E: RANKL and OPG expression and protein release into the supernatant is determined using osteoblasts (WT or Syndecan-1-/-) cultured in DM or DM+ medium. Experiments were performed in independent triplicates (A; B, E) or duplicates (D), data are displayed as mean ± SD.
    Figure Legend Snippet: Expression of Syndecan-1 in osteoblasts and osteoclasts during differentiation in vitro.. Co-cultures of osteoblasts and osteoclasts were performed in presence of 1,25(OH) 2 D 3 and PGE2 (DM+, see Table 1 ). AB: mRNA expression of Syndecan-1-4 were analysed using quantitative realtime PCR (Primers see Table 2 ) normalized to HPRT and day 1 of culture (ΔΔCT method). C: Protein expression of Syndecan-1 in the cells was detected using a polyclonal antibody against Syndecan-1. Scale bar: 50µm. D: Syndecan-1 expression was analysed after stimulation of osteoblastic cells with DM+ medium. mRNA expression was determined by realtime PCR (left). The concentration of soluble Syndecan-1 protein in the supernatant of cells was analysed by ELISA (right). E: RANKL and OPG expression and protein release into the supernatant is determined using osteoblasts (WT or Syndecan-1-/-) cultured in DM or DM+ medium. Experiments were performed in independent triplicates (A; B, E) or duplicates (D), data are displayed as mean ± SD.

    Techniques Used: Expressing, In Vitro, Polymerase Chain Reaction, Concentration Assay, Enzyme-linked Immunosorbent Assay, Cell Culture

    24) Product Images from "Critical role of OX40 in drug‐induced acute liver injury, et al. Critical role of OX40 in drug‐induced acute liver injury"

    Article Title: Critical role of OX40 in drug‐induced acute liver injury, et al. Critical role of OX40 in drug‐induced acute liver injury

    Journal: British Journal of Pharmacology

    doi: 10.1111/bph.15041

    Soluble OX40 stimulation enhances the pro‐inflammatory state of murine macrophage. (a) Expression of antigen presentation‐associated molecules and chemokine receptors in RAW264.7 cells, determined by flow cytometry, and quantitative real‐time PCR analysis of the pro‐inflammatory cytokine mRNA levels in OX40/Fc‐stimulated RAW264.7 cells. (b) Expression of antigen presentation‐associated molecules and chemokine receptors in J774A.1 cells, determined by flow cytometry, and quantitative real‐time PCR analysis of the pro‐inflammatory cytokine mRNA levels in OX40/Fc‐stimulated J774A.1 cells. (c) Representative flow cytometry images of hypoxia‐inducible factor 1 alpha (Hif1α + ) population among OX40/Fc‐stimulated RAW264.7 and J774A.1 cells. (d) Relative changes in Hif1α expression, plotted as fold changes of Hif1α expressed in the IgG‐treated group. (e) Quantitative real‐time PCR analysis of Hif1a mRNA level in OX40/Fc‐stimulated RAW264.7 and J774A.1 cells. (f) Plasma soluble OX40 levels determined by ELISA in HC and drug‐induced liver injury (DILI) patients. (g) Evidence of significant positive correlation between the plasma OX40 and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL) and direct bilirubin (DBIL) levels and lack of significant correlation between the plasma OX40 and albumin (ALB) levels ( n = 26). The data are presented as the mean ± SEM. Two‐group comparisons were made by the unpaired Student's t‐ test, and multiple comparisons were analysed by one‐way ANOVA followed by Bonferronis's post hoc test. While for the clinical study data, normal variable distributions were tested using the Shapiro–Wilk test. Spearman's correlation coefficient was used to estimate the association of plasma OX40 levels and ALT, AST, TBIL, DBIL and ALB. * P
    Figure Legend Snippet: Soluble OX40 stimulation enhances the pro‐inflammatory state of murine macrophage. (a) Expression of antigen presentation‐associated molecules and chemokine receptors in RAW264.7 cells, determined by flow cytometry, and quantitative real‐time PCR analysis of the pro‐inflammatory cytokine mRNA levels in OX40/Fc‐stimulated RAW264.7 cells. (b) Expression of antigen presentation‐associated molecules and chemokine receptors in J774A.1 cells, determined by flow cytometry, and quantitative real‐time PCR analysis of the pro‐inflammatory cytokine mRNA levels in OX40/Fc‐stimulated J774A.1 cells. (c) Representative flow cytometry images of hypoxia‐inducible factor 1 alpha (Hif1α + ) population among OX40/Fc‐stimulated RAW264.7 and J774A.1 cells. (d) Relative changes in Hif1α expression, plotted as fold changes of Hif1α expressed in the IgG‐treated group. (e) Quantitative real‐time PCR analysis of Hif1a mRNA level in OX40/Fc‐stimulated RAW264.7 and J774A.1 cells. (f) Plasma soluble OX40 levels determined by ELISA in HC and drug‐induced liver injury (DILI) patients. (g) Evidence of significant positive correlation between the plasma OX40 and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL) and direct bilirubin (DBIL) levels and lack of significant correlation between the plasma OX40 and albumin (ALB) levels ( n = 26). The data are presented as the mean ± SEM. Two‐group comparisons were made by the unpaired Student's t‐ test, and multiple comparisons were analysed by one‐way ANOVA followed by Bonferronis's post hoc test. While for the clinical study data, normal variable distributions were tested using the Shapiro–Wilk test. Spearman's correlation coefficient was used to estimate the association of plasma OX40 levels and ALT, AST, TBIL, DBIL and ALB. * P

    Techniques Used: Expressing, Flow Cytometry, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, AST Assay

    Ox40 deficiency attenuates liver injury after paracetamol (APAP) overdose. Acute liver injury (ALI) was induced in C57BL/6 WT by i.p. injecting 150, 200, 250 or 300 mg·kg −1 paracetamol. The control animals were injected the same volume of PBS. (a) Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) plasma levels 12, 24, 48 and 72 hr after paracetamol injection. (b) ALT and AST plasma levels 24 hr after APAP challenge. (c) Soluble OX40 levels were determined by ELISA in PBS and APAP with four doses. (d) Ox40 mRNA level in hepatic mononuclear cell (MNCs) from the PBS group and 300 mg·kg −1 APAP group. (e) Representative flow cytometry images of OX40 + cells among intrahepatic NK, NKT, CD4 + and CD8 + T cells. (f) Statistical analysis of OX40 levels in intrahepatic NK, NKT, CD4 + and CD8 + T cells, as determined by flow cytometry. (g) ALT and AST plasma levels at 24 hr after injection of 300 mg·kg −1 APAP. (h) Liver histology (H E staining) 24 hr after administration of 300 mg·kg −1 APAP. Centrilobular necrosis, bridging necrosis, and massive hepatocyte death are apparent. Original magnification, 100×; scale bar, 200 μm. (i) Relative levels of pro‐inflammatory cytokine mRNA in liver tissue, analysed by quantitative real‐time PCR. (j) Hepatic GSH levels. (k,l) Western blot analysis of CTP2E1 in liver tissue. The data are presented as the mean ± SEM; control groups ( n = 5) and treatment groups ( n = 6). Two‐group comparisons were made by the Student's t test, and multiple comparisons were analysed by one‐way ANOVA followed by Bonferronis's post hoc test. * P
    Figure Legend Snippet: Ox40 deficiency attenuates liver injury after paracetamol (APAP) overdose. Acute liver injury (ALI) was induced in C57BL/6 WT by i.p. injecting 150, 200, 250 or 300 mg·kg −1 paracetamol. The control animals were injected the same volume of PBS. (a) Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) plasma levels 12, 24, 48 and 72 hr after paracetamol injection. (b) ALT and AST plasma levels 24 hr after APAP challenge. (c) Soluble OX40 levels were determined by ELISA in PBS and APAP with four doses. (d) Ox40 mRNA level in hepatic mononuclear cell (MNCs) from the PBS group and 300 mg·kg −1 APAP group. (e) Representative flow cytometry images of OX40 + cells among intrahepatic NK, NKT, CD4 + and CD8 + T cells. (f) Statistical analysis of OX40 levels in intrahepatic NK, NKT, CD4 + and CD8 + T cells, as determined by flow cytometry. (g) ALT and AST plasma levels at 24 hr after injection of 300 mg·kg −1 APAP. (h) Liver histology (H E staining) 24 hr after administration of 300 mg·kg −1 APAP. Centrilobular necrosis, bridging necrosis, and massive hepatocyte death are apparent. Original magnification, 100×; scale bar, 200 μm. (i) Relative levels of pro‐inflammatory cytokine mRNA in liver tissue, analysed by quantitative real‐time PCR. (j) Hepatic GSH levels. (k,l) Western blot analysis of CTP2E1 in liver tissue. The data are presented as the mean ± SEM; control groups ( n = 5) and treatment groups ( n = 6). Two‐group comparisons were made by the Student's t test, and multiple comparisons were analysed by one‐way ANOVA followed by Bonferronis's post hoc test. * P

    Techniques Used: Injection, AST Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Staining, Real-time Polymerase Chain Reaction, Western Blot

    25) Product Images from "GHK Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice by Suppressing TGFβ1/Smad-Mediated Epithelial-to-Mesenchymal Transition"

    Article Title: GHK Peptide Inhibits Bleomycin-Induced Pulmonary Fibrosis in Mice by Suppressing TGFβ1/Smad-Mediated Epithelial-to-Mesenchymal Transition

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2017.00904

    Effects of GHK on TGF-β1 mRNA and protein expression in mice with BLM-induced fibrosis. (A) TGF-β1 expression levels in lung tissues in each group were determined by real-time PCR. (B) TGF-β1 activity in lung tissues was measured by an ELISA kit. (C) TGF-β1 protein expression in lung tissues in each group was measured by western blot analysis. (D) The densitometry values of the proteins were normalized to those of β-actin. All data represent the mean ± SEM of three independent experiments performed in triplicate. Statistical analysis was performed by one-way ANOVA and Turkey’s multiple-comparison test; compared with control group, ## P
    Figure Legend Snippet: Effects of GHK on TGF-β1 mRNA and protein expression in mice with BLM-induced fibrosis. (A) TGF-β1 expression levels in lung tissues in each group were determined by real-time PCR. (B) TGF-β1 activity in lung tissues was measured by an ELISA kit. (C) TGF-β1 protein expression in lung tissues in each group was measured by western blot analysis. (D) The densitometry values of the proteins were normalized to those of β-actin. All data represent the mean ± SEM of three independent experiments performed in triplicate. Statistical analysis was performed by one-way ANOVA and Turkey’s multiple-comparison test; compared with control group, ## P

    Techniques Used: Expressing, Mouse Assay, Real-time Polymerase Chain Reaction, Activity Assay, Enzyme-linked Immunosorbent Assay, Western Blot

    26) Product Images from "Akebia saponin D protects hippocampal neurogenesis from microglia-mediated inflammation and ameliorates depressive-like behaviors and cognitive impairment in mice through the PI3K-Akt pathway"

    Article Title: Akebia saponin D protects hippocampal neurogenesis from microglia-mediated inflammation and ameliorates depressive-like behaviors and cognitive impairment in mice through the PI3K-Akt pathway

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2022.927419

    ASD activates the PI3K-Akt pathway in hippocampus of mice chronically exposed to LPS. (A) , Scheme of the experimental procedure. ASD, akebia saponin D; DMSO, dimethyl sulphoxide; ELISA, enzyme-linked immunosorbent assay; EPMT, elevated plus maze test; FST, forced swimming test; IHC, immunocytochemistry; LPS, lipopolysaccharide; Mino, minocycline; NORT, novel object recognition test; SPT, sucrose preference test; WB, western blotting. (B,C) , Western blotting shows the levels of PI3K and pAkt in the hippocampus of mice treated with saline (Ctrl) or lipopolysaccharide (LPS), then with akebia saponin D (ASD), minocycline (Mino) or PI3K-Akt inhibitor (LY294002). Levels of PI3K were normalized to those of β-actin, and levels of pAkt were normalized to those of Akt. Data are mean ± standard error of the mean (SEM) (n = 4), *** p
    Figure Legend Snippet: ASD activates the PI3K-Akt pathway in hippocampus of mice chronically exposed to LPS. (A) , Scheme of the experimental procedure. ASD, akebia saponin D; DMSO, dimethyl sulphoxide; ELISA, enzyme-linked immunosorbent assay; EPMT, elevated plus maze test; FST, forced swimming test; IHC, immunocytochemistry; LPS, lipopolysaccharide; Mino, minocycline; NORT, novel object recognition test; SPT, sucrose preference test; WB, western blotting. (B,C) , Western blotting shows the levels of PI3K and pAkt in the hippocampus of mice treated with saline (Ctrl) or lipopolysaccharide (LPS), then with akebia saponin D (ASD), minocycline (Mino) or PI3K-Akt inhibitor (LY294002). Levels of PI3K were normalized to those of β-actin, and levels of pAkt were normalized to those of Akt. Data are mean ± standard error of the mean (SEM) (n = 4), *** p

    Techniques Used: Mouse Assay, Enzyme-linked Immunosorbent Assay, Immunohistochemistry, Immunocytochemistry, Single-particle Tracking, Western Blot

    27) Product Images from "Total flavonoids of hawthorn leaves protect spinal motor neurons via promotion of autophagy after spinal cord injury"

    Article Title: Total flavonoids of hawthorn leaves protect spinal motor neurons via promotion of autophagy after spinal cord injury

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2022.925568

    TFHL promotes secretion of neurotrophic factors by astrocytes. (A–D) The secretion of BDNF, GDNF, NGF, and CNTF in each group was detected by ELISA. The comparison of the contents of BDNF, GDNF, NGF, and CNTF in the culture medium of each group. All data are expressed as the mean ± SD. Differences among groups were determined with one-way ANOVA followed by a least-significant difference post hoc test. * p
    Figure Legend Snippet: TFHL promotes secretion of neurotrophic factors by astrocytes. (A–D) The secretion of BDNF, GDNF, NGF, and CNTF in each group was detected by ELISA. The comparison of the contents of BDNF, GDNF, NGF, and CNTF in the culture medium of each group. All data are expressed as the mean ± SD. Differences among groups were determined with one-way ANOVA followed by a least-significant difference post hoc test. * p

    Techniques Used: Enzyme-linked Immunosorbent Assay

    28) Product Images from "SOCS2 overexpression alleviates diabetic nephropathy in rats by inhibiting the TLR4/NF-κB pathway"

    Article Title: SOCS2 overexpression alleviates diabetic nephropathy in rats by inhibiting the TLR4/NF-κB pathway

    Journal: Oncotarget

    doi: 10.18632/oncotarget.20434

    Effect of SOCS2 overexpression on the generation of IL-6, IL-1β and MCP-1 in STZ-induced DN rats The levels of IL-6, IL-1β and MCP-1 in blood (A, B and C) and kidney cortex (D, E and F) of control rats, DN rats or DN rats infected with Ad-GFP or Ad-SOCS2 were examined by ELISA. * P
    Figure Legend Snippet: Effect of SOCS2 overexpression on the generation of IL-6, IL-1β and MCP-1 in STZ-induced DN rats The levels of IL-6, IL-1β and MCP-1 in blood (A, B and C) and kidney cortex (D, E and F) of control rats, DN rats or DN rats infected with Ad-GFP or Ad-SOCS2 were examined by ELISA. * P

    Techniques Used: Over Expression, Infection, Enzyme-linked Immunosorbent Assay

    29) Product Images from "Loss of the androgen receptor suppresses intrarenal calcium oxalate crystals deposition via altering macrophage recruitment/M2 polarization with change of the miR-185-5p/CSF-1 signals"

    Article Title: Loss of the androgen receptor suppresses intrarenal calcium oxalate crystals deposition via altering macrophage recruitment/M2 polarization with change of the miR-185-5p/CSF-1 signals

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-019-1358-y

    Loss of androgen receptor (AR) increased renal CSF-1 expression and M2 macrophage infiltration in glyoxylate-induced intrarenal calcium oxalate (CaOx) crystals deposition mouse model. a The quantitative real-time PCR (qRT-PCR) analysis of CSF-1 gene and miR-185-5p expression in mice kidneys. b (IHC staining of mouse kidney tissues showing that loss of AR in Cdh16-ARKO mice increased the CSF-1 expression. Quantification of CSF-1 positive renal tubules is shown in the right panel. c Kidney CSF-1 levels in WT and Cdh16-ARKO mice. CSF-1 levels in kidney homogenates determined by ELISA. d Representative MISH staining results for mmu-miR-185-5p in kidney tissues from WT or Cdh16-ARKO mice. e AR deletion in the renal tubule led to increased mRNA levels of markers of pan-MΦs and M2-like MΦs, including F4/80, CD163, CD206 (mannose receptor), but not INOS, in kidneys from mice with glyoxylate injection for 6 days. f Immunostaining indicated increased renal F4/80-positive MΦs in the renal corticomedullary junction from Cdh16-ARKO mice at 6 days after glyoxylate injection. g Immunostaining indicated increased renal CD163-positive MΦs in the renal corticomedullary junction from Cdh16-ARKO mice at 6 days after glyoxylate injection. h Immunofluorescence indicated increased renal CD206-positive MΦs in the Cdh16-ARKO mice at 6 days after glyoxylate injection. For B, D, F, G and H, quantitations are at the right and all quantitations are mean ± SD, * P
    Figure Legend Snippet: Loss of androgen receptor (AR) increased renal CSF-1 expression and M2 macrophage infiltration in glyoxylate-induced intrarenal calcium oxalate (CaOx) crystals deposition mouse model. a The quantitative real-time PCR (qRT-PCR) analysis of CSF-1 gene and miR-185-5p expression in mice kidneys. b (IHC staining of mouse kidney tissues showing that loss of AR in Cdh16-ARKO mice increased the CSF-1 expression. Quantification of CSF-1 positive renal tubules is shown in the right panel. c Kidney CSF-1 levels in WT and Cdh16-ARKO mice. CSF-1 levels in kidney homogenates determined by ELISA. d Representative MISH staining results for mmu-miR-185-5p in kidney tissues from WT or Cdh16-ARKO mice. e AR deletion in the renal tubule led to increased mRNA levels of markers of pan-MΦs and M2-like MΦs, including F4/80, CD163, CD206 (mannose receptor), but not INOS, in kidneys from mice with glyoxylate injection for 6 days. f Immunostaining indicated increased renal F4/80-positive MΦs in the renal corticomedullary junction from Cdh16-ARKO mice at 6 days after glyoxylate injection. g Immunostaining indicated increased renal CD163-positive MΦs in the renal corticomedullary junction from Cdh16-ARKO mice at 6 days after glyoxylate injection. h Immunofluorescence indicated increased renal CD206-positive MΦs in the Cdh16-ARKO mice at 6 days after glyoxylate injection. For B, D, F, G and H, quantitations are at the right and all quantitations are mean ± SD, * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Mouse Assay, Immunohistochemistry, Staining, Enzyme-linked Immunosorbent Assay, Injection, Immunostaining, Immunofluorescence

    Knocking down androgen receptor (AR) in renal tubular epithelial cells (RTCs) enhanced the macrophages migration and M2 polarization via modulating the CSF-1 signals. a-c Cells were pre-treated with shAR or with scrambled control (scr). After 72-h incubation, cells were treated with 20 μg/cm 2 COM crystals for 24 h. a Quantitative real-time PCR (qRT-PCR) analysis of MΦs-associated cytokines in HK-2 and HKC-8 cells with/without knockdown of AR. b The level of CSF-1 in the CM of RTCs was detected by ELISA. c The level of CSF-1 in the RTCs lysates was detected by western blot. d qRT-PCR (left panels) and western blot (right panels) show CSF-1 knockdown efficiency in HK-2 and HKC-8 cells. e Knocking down AR in HK-2 and HKC-8 cells increased M0-MΦs migration, whereas knocking down CSF-1 interrupted the AR knockdown-mediated increase of M0-MΦs migration. f CM from AR-depleted RTCs led to increase mRNA levels of markers of M2 phenotypic MΦs (CD163 and CD206), whereas knocking down CSF-1 in RTCs interrupted AR knockdown-mediated M2-MΦs markers change. g Flow cytometry analysis showed that CM from AR-depleted RTCs led to increase expressions markers of M2 phenotypic MΦs (CD163 and CD206), whereas knocking down CSF-1 in RTCs interrupted AR knockdown-mediated M2-MΦs markers change. h Knocking down CSF-1 in HK-2 and HKC-8 partly reversed the AR knockdown-enhanced COM crystals phagocytic ability of MΦs. For e, g and h , quantifications are at the right. All quantitations are presented as mean ± SD. * P
    Figure Legend Snippet: Knocking down androgen receptor (AR) in renal tubular epithelial cells (RTCs) enhanced the macrophages migration and M2 polarization via modulating the CSF-1 signals. a-c Cells were pre-treated with shAR or with scrambled control (scr). After 72-h incubation, cells were treated with 20 μg/cm 2 COM crystals for 24 h. a Quantitative real-time PCR (qRT-PCR) analysis of MΦs-associated cytokines in HK-2 and HKC-8 cells with/without knockdown of AR. b The level of CSF-1 in the CM of RTCs was detected by ELISA. c The level of CSF-1 in the RTCs lysates was detected by western blot. d qRT-PCR (left panels) and western blot (right panels) show CSF-1 knockdown efficiency in HK-2 and HKC-8 cells. e Knocking down AR in HK-2 and HKC-8 cells increased M0-MΦs migration, whereas knocking down CSF-1 interrupted the AR knockdown-mediated increase of M0-MΦs migration. f CM from AR-depleted RTCs led to increase mRNA levels of markers of M2 phenotypic MΦs (CD163 and CD206), whereas knocking down CSF-1 in RTCs interrupted AR knockdown-mediated M2-MΦs markers change. g Flow cytometry analysis showed that CM from AR-depleted RTCs led to increase expressions markers of M2 phenotypic MΦs (CD163 and CD206), whereas knocking down CSF-1 in RTCs interrupted AR knockdown-mediated M2-MΦs markers change. h Knocking down CSF-1 in HK-2 and HKC-8 partly reversed the AR knockdown-enhanced COM crystals phagocytic ability of MΦs. For e, g and h , quantifications are at the right. All quantitations are presented as mean ± SD. * P

    Techniques Used: Migration, Incubation, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Western Blot, Flow Cytometry, Cytometry

    Androgen receptor (AR) modulates CSF-1 via upregulation of miR-185-5p in renal tubular epithelial cells (RTCs) exposed to calcium oxalate monohydrate (COM) crystals. a Eighteen potential miRNAs candidates were screened by quantitative real-time PCR (qRT-PCR) assay in HK-2 cells and HKC-8 cells based on their response to knocking down AR. Cells were pre-treated with 20 μg/cm 2 COM crystals for 24 h. b The qRT-PCR analysis of five miRNAs in both HK-2 and HKC-8 cells with shAR compared with control. c, d HK-2 and HKC-8 cells were virally transduced with miR-15a-5p, miR-130b-3p, miR-185-5p, miR-650, and miR-1207-5p. Cells were then exposed to 20 μg/cm 2 COM crystals for 24 h. Total RNAs ( c ) were analyzed for CSF-1 by qRT-PCR. The protein expression levels ( d ) of CSF-1 in the CM of HK-2 and HKC-8 cells were assessed by ELISA. e The mRNA levels of CSF-1 were determined by qRT-PCR analysis after co-transfection with shAR and miR-185-5p (vs. scramble). f The protein levels of CSF-1 in RTCs CM were determined by ELISA after co-transfection with shAR and miR-185-5p (vs. scramble). g M0-MΦs migration to the CM from HK-2 cells (upper) and HKC-8 cells (lower) with four groups (scramble, shAR, miR-185-5p, and shAR + miR-185-5p). h Overexpressing miR-185-5p in HK-2 cells and HKC-8 cells partly reversed the AR knockdown-enhanced COM crystals phagocytic ability of MΦs. For g and h , quantifications are at the right. All quantitations are presented as mean ± SD. * P
    Figure Legend Snippet: Androgen receptor (AR) modulates CSF-1 via upregulation of miR-185-5p in renal tubular epithelial cells (RTCs) exposed to calcium oxalate monohydrate (COM) crystals. a Eighteen potential miRNAs candidates were screened by quantitative real-time PCR (qRT-PCR) assay in HK-2 cells and HKC-8 cells based on their response to knocking down AR. Cells were pre-treated with 20 μg/cm 2 COM crystals for 24 h. b The qRT-PCR analysis of five miRNAs in both HK-2 and HKC-8 cells with shAR compared with control. c, d HK-2 and HKC-8 cells were virally transduced with miR-15a-5p, miR-130b-3p, miR-185-5p, miR-650, and miR-1207-5p. Cells were then exposed to 20 μg/cm 2 COM crystals for 24 h. Total RNAs ( c ) were analyzed for CSF-1 by qRT-PCR. The protein expression levels ( d ) of CSF-1 in the CM of HK-2 and HKC-8 cells were assessed by ELISA. e The mRNA levels of CSF-1 were determined by qRT-PCR analysis after co-transfection with shAR and miR-185-5p (vs. scramble). f The protein levels of CSF-1 in RTCs CM were determined by ELISA after co-transfection with shAR and miR-185-5p (vs. scramble). g M0-MΦs migration to the CM from HK-2 cells (upper) and HKC-8 cells (lower) with four groups (scramble, shAR, miR-185-5p, and shAR + miR-185-5p). h Overexpressing miR-185-5p in HK-2 cells and HKC-8 cells partly reversed the AR knockdown-enhanced COM crystals phagocytic ability of MΦs. For g and h , quantifications are at the right. All quantitations are presented as mean ± SD. * P

    Techniques Used: Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Transduction, Expressing, Enzyme-linked Immunosorbent Assay, Cotransfection, Migration

    30) Product Images from "MicroRNA-155-5p modulates the progression of acute respiratory distress syndrome by targeting interleukin receptors"

    Article Title: MicroRNA-155-5p modulates the progression of acute respiratory distress syndrome by targeting interleukin receptors

    Journal: Bioengineered

    doi: 10.1080/21655979.2022.2071020

    Upregulated levels of the inflammatory cytokines in patients with ARDS. The levels of IL17RB, IL18R1, and IL22RA2 in serum samples from patients with ARDS (a). Serum concentrations of IL17RB, IL18R1, and IL22RA2 (b), and IL-1β, IL-6, IL-8, and TNF-α (c) in patients with ARDS were analyzed by ELISA. *p
    Figure Legend Snippet: Upregulated levels of the inflammatory cytokines in patients with ARDS. The levels of IL17RB, IL18R1, and IL22RA2 in serum samples from patients with ARDS (a). Serum concentrations of IL17RB, IL18R1, and IL22RA2 (b), and IL-1β, IL-6, IL-8, and TNF-α (c) in patients with ARDS were analyzed by ELISA. *p

    Techniques Used: Enzyme-linked Immunosorbent Assay

    31) Product Images from "The heparan sulfate proteoglycan Syndecan-1 influences local bone cell communication via the RANKL/OPG axis"

    Article Title: The heparan sulfate proteoglycan Syndecan-1 influences local bone cell communication via the RANKL/OPG axis

    Journal: bioRxiv

    doi: 10.1101/852590

    Influence of Syndecan-1 deficiency on serum concentration of RANKL and OPG and bone structure in mice during aging. A, B, C : Serum was collected from female mice (WT (all), Syndecan-1 KO (only in B , C )) of 4, 12 and 18 month of age and concentration of Syndecan-1 ( A ), RANKL ( B ) and OPG ( C ) was determined by ELISA. Data are displayed as mean ± SD, Kruskal-Wallis test with Dunn’s post hoc test, n =9-13 per group. *p
    Figure Legend Snippet: Influence of Syndecan-1 deficiency on serum concentration of RANKL and OPG and bone structure in mice during aging. A, B, C : Serum was collected from female mice (WT (all), Syndecan-1 KO (only in B , C )) of 4, 12 and 18 month of age and concentration of Syndecan-1 ( A ), RANKL ( B ) and OPG ( C ) was determined by ELISA. Data are displayed as mean ± SD, Kruskal-Wallis test with Dunn’s post hoc test, n =9-13 per group. *p

    Techniques Used: Concentration Assay, Mouse Assay, Enzyme-linked Immunosorbent Assay

    Syndecan-1, RANKL and OPG expression was analysed after stimulation of osteoblastic cells with DM or DM+ medium (day 7). A : mRNA expression of Syndecan-1 (in WT cells) was determined by real time PCR. B, C : The concentration of soluble Syndecan-1 protein in the supernatant ( B ) and cell layer ( C ) of cells (WT) was analysed by ELISA. Experiments were performed in triplicates. Mann-Whitney-U test, *p
    Figure Legend Snippet: Syndecan-1, RANKL and OPG expression was analysed after stimulation of osteoblastic cells with DM or DM+ medium (day 7). A : mRNA expression of Syndecan-1 (in WT cells) was determined by real time PCR. B, C : The concentration of soluble Syndecan-1 protein in the supernatant ( B ) and cell layer ( C ) of cells (WT) was analysed by ELISA. Experiments were performed in triplicates. Mann-Whitney-U test, *p

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Concentration Assay, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

    32) Product Images from "Compound hemizygous variants in SERPINA7 gene cause thyroxine‐binding globulin deficiency"

    Article Title: Compound hemizygous variants in SERPINA7 gene cause thyroxine‐binding globulin deficiency

    Journal: Molecular Genetics & Genomic Medicine

    doi: 10.1002/mgg3.1571

    Extracellular and intracellular TBG levels. (a and b) Detection of extracellular TBG secretion by ELISA. The genotypes of the TBG‐CD patients are filled with red, the genotypes of the TBG‐PD patients are filled with orange, and the wild type is filled with black color. (c and d) The protein expression level was measured by Western blot analysis. The data are presented as the means ±SDs, * p
    Figure Legend Snippet: Extracellular and intracellular TBG levels. (a and b) Detection of extracellular TBG secretion by ELISA. The genotypes of the TBG‐CD patients are filled with red, the genotypes of the TBG‐PD patients are filled with orange, and the wild type is filled with black color. (c and d) The protein expression level was measured by Western blot analysis. The data are presented as the means ±SDs, * p

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing, Western Blot

    33) Product Images from "Heme oxygenase-1 attenuates IL-1β induced alteration of anabolic and catabolic activities in intervertebral disc degeneration"

    Article Title: Heme oxygenase-1 attenuates IL-1β induced alteration of anabolic and catabolic activities in intervertebral disc degeneration

    Journal: Scientific Reports

    doi: 10.1038/srep21190

    Effects of HO-1 induction by CoPP on expression of ECM catabolic genes in human NP cells Real-time PCR revealed that the induction of gene expression of the ECM catabolic enzymes MMP-1 ( a ), MMP-3 ( b ), MMP-9 ( c ), MMP-13 ( d ), ADAMTS-5 ( e ) and ADAMTS-4 ( f ) by IL-1β treatment was ameliorated by the HO-1 inducer CoPP. Treatment with CoPP alone did not affect the basal levels of expression of these catabolic genes ( P > 0.05). ELISA showed that IL-1β stimulation of the protein levels of MMP-1 ( g ), MMP-3 ( h ), MMP-9 ( i ) and MMP-13 ( j ) were attenuated by induction of HO-1. The data also showed that treatment with CoPP alone downregulated the basal protein levels of MMP-1, MMP-3, MMP-9 and MMP-13. Values represent the mean and SD. * P
    Figure Legend Snippet: Effects of HO-1 induction by CoPP on expression of ECM catabolic genes in human NP cells Real-time PCR revealed that the induction of gene expression of the ECM catabolic enzymes MMP-1 ( a ), MMP-3 ( b ), MMP-9 ( c ), MMP-13 ( d ), ADAMTS-5 ( e ) and ADAMTS-4 ( f ) by IL-1β treatment was ameliorated by the HO-1 inducer CoPP. Treatment with CoPP alone did not affect the basal levels of expression of these catabolic genes ( P > 0.05). ELISA showed that IL-1β stimulation of the protein levels of MMP-1 ( g ), MMP-3 ( h ), MMP-9 ( i ) and MMP-13 ( j ) were attenuated by induction of HO-1. The data also showed that treatment with CoPP alone downregulated the basal protein levels of MMP-1, MMP-3, MMP-9 and MMP-13. Values represent the mean and SD. * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

    34) Product Images from "TGFβ3-mediated induction of Periostin facilitates head and neck cancer growth and is associated with metastasis"

    Article Title: TGFβ3-mediated induction of Periostin facilitates head and neck cancer growth and is associated with metastasis

    Journal: Scientific Reports

    doi: 10.1038/srep20587

    CAFs contributed to the overexpression of POSTN in HNC tissues. ( A,B ) The transcriptional and translational statuses of POSTN were determined in CAFs and NFs, 6 representative HNC cell lines and normal oral epithelial cells (titled normal) using western blotting ( A ) and real-time PCR ( B ). ( C ) Representative images of immunohistochemical staining showed the distribution of POSTN expression in adjacent normal tissues and HNC tissues. ( D,E ) POSTN expressions in NFs and CAFs were detected using immunohistochemical staining ( D ) and confocal microscopy ( E ). ( F ) The protein levels of POSTN, FAP and α-SMA were determined by a western blot analysis. ( G ) POSTN mRNA levels in 5 pairs of NFs and CAFs were measured by real-time PCR. ( H ) POSTN protein levels in the media of NFs and CAFs were determined by ELISA analyses. (**** p
    Figure Legend Snippet: CAFs contributed to the overexpression of POSTN in HNC tissues. ( A,B ) The transcriptional and translational statuses of POSTN were determined in CAFs and NFs, 6 representative HNC cell lines and normal oral epithelial cells (titled normal) using western blotting ( A ) and real-time PCR ( B ). ( C ) Representative images of immunohistochemical staining showed the distribution of POSTN expression in adjacent normal tissues and HNC tissues. ( D,E ) POSTN expressions in NFs and CAFs were detected using immunohistochemical staining ( D ) and confocal microscopy ( E ). ( F ) The protein levels of POSTN, FAP and α-SMA were determined by a western blot analysis. ( G ) POSTN mRNA levels in 5 pairs of NFs and CAFs were measured by real-time PCR. ( H ) POSTN protein levels in the media of NFs and CAFs were determined by ELISA analyses. (**** p

    Techniques Used: Over Expression, Western Blot, Real-time Polymerase Chain Reaction, Immunohistochemistry, Staining, Expressing, Confocal Microscopy, Enzyme-linked Immunosorbent Assay

    35) Product Images from "Dexmedetomidine Alleviates Neuropathic Pain via the TRPC6-p38 MAPK Pathway in the Dorsal Root Ganglia of Rats"

    Article Title: Dexmedetomidine Alleviates Neuropathic Pain via the TRPC6-p38 MAPK Pathway in the Dorsal Root Ganglia of Rats

    Journal: Journal of Pain Research

    doi: 10.2147/JPR.S378893

    The levels of proinflammatory cytokines were downregulated after 7 days of dexmedetomidine administration in the ipsilateral DRG. ( A ) The concentration of TNF-α in each group was detected using the ELISA kit. The increased expression of TNF-α was significantly reduced by Dex in the DRG. ( B ) The concentration of IL-1β in the three groups. The concentration of IL-1β was increased in the CCI-NS group, which was suppressed by Dex. ** p
    Figure Legend Snippet: The levels of proinflammatory cytokines were downregulated after 7 days of dexmedetomidine administration in the ipsilateral DRG. ( A ) The concentration of TNF-α in each group was detected using the ELISA kit. The increased expression of TNF-α was significantly reduced by Dex in the DRG. ( B ) The concentration of IL-1β in the three groups. The concentration of IL-1β was increased in the CCI-NS group, which was suppressed by Dex. ** p

    Techniques Used: Concentration Assay, Enzyme-linked Immunosorbent Assay, Expressing

    36) Product Images from "Kallikrein 6 protease advances colon tumorigenesis via induction of the high mobility group A2 protein"

    Article Title: Kallikrein 6 protease advances colon tumorigenesis via induction of the high mobility group A2 protein

    Journal: Oncotarget

    doi: 10.18632/oncotarget.27153

    KLK6 enzyme contributes to cell invasion in HCT116-shKLK6 model through induction of the EMT. ( A ). KLK6 enzymatic activity is required for invasive phenotype of HCT116 cells. Upper panel: Cell invasion through Matrigel following transient transfection of KLK6 wt or KLK6 S197A plasmids into HCT116 control clone 1 and shKLK6 clone 3. Cells were seeded in Matrigel invasion chambers 24 h after transfection and were analyzed 48 h later. HCT116 Control clone 1 untransfected and co-transfected with pcDNA3.1 vector served as controls. * p = 0.0004 (shKLK6 +pcDNA3.1 vs shKLK6+wt KLK6), ** p = 0.0008 (shKLK6-3/KLK6 wt vs shKLK6/KLK6) S197A, by t -test. This figure is representative of two independent experiments performed in sextuplets with error bar indicating SD. Middle panel: Secreted KLK6 protein levels in conditioned media by ELISA from Matrigel invasion assay (upper panel), *** p = 0.0002 and ** p = 0.0008 (shKLK6+wt KLK6 vs shKLK6+KLK6 KLK6 S197A), by paired t -test, respectively. Lower panel. Analysis of secreted active TGF-β2 protein in the conditioned media from Matrigel invasion assay. Figures are representative of two independent experiments performed with triplicates. Error bars indicate SD. ( B ) Levels of ZO1, E cadherin and Snail in HCT-shKLK6 cell model. RIU: relative intensity units, quantification was done using Image J. Bands of the protein of interest were normalized to β-actin. The proteins sizes are indicated in kilodalton (kDa). Images are representative of three independent experiments.
    Figure Legend Snippet: KLK6 enzyme contributes to cell invasion in HCT116-shKLK6 model through induction of the EMT. ( A ). KLK6 enzymatic activity is required for invasive phenotype of HCT116 cells. Upper panel: Cell invasion through Matrigel following transient transfection of KLK6 wt or KLK6 S197A plasmids into HCT116 control clone 1 and shKLK6 clone 3. Cells were seeded in Matrigel invasion chambers 24 h after transfection and were analyzed 48 h later. HCT116 Control clone 1 untransfected and co-transfected with pcDNA3.1 vector served as controls. * p = 0.0004 (shKLK6 +pcDNA3.1 vs shKLK6+wt KLK6), ** p = 0.0008 (shKLK6-3/KLK6 wt vs shKLK6/KLK6) S197A, by t -test. This figure is representative of two independent experiments performed in sextuplets with error bar indicating SD. Middle panel: Secreted KLK6 protein levels in conditioned media by ELISA from Matrigel invasion assay (upper panel), *** p = 0.0002 and ** p = 0.0008 (shKLK6+wt KLK6 vs shKLK6+KLK6 KLK6 S197A), by paired t -test, respectively. Lower panel. Analysis of secreted active TGF-β2 protein in the conditioned media from Matrigel invasion assay. Figures are representative of two independent experiments performed with triplicates. Error bars indicate SD. ( B ) Levels of ZO1, E cadherin and Snail in HCT-shKLK6 cell model. RIU: relative intensity units, quantification was done using Image J. Bands of the protein of interest were normalized to β-actin. The proteins sizes are indicated in kilodalton (kDa). Images are representative of three independent experiments.

    Techniques Used: Activity Assay, Transfection, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Invasion Assay

    37) Product Images from "Arctiin attenuates high glucose‐induced human retinal capillary endothelial cell proliferation by regulating ROCK1/PTEN/PI3K/Akt/VEGF pathway in vitro. Arctiin attenuates high glucose‐induced human retinal capillary endothelial cell proliferation by regulating ROCK1/PTEN/PI3K/Akt/VEGF pathway in vitro"

    Article Title: Arctiin attenuates high glucose‐induced human retinal capillary endothelial cell proliferation by regulating ROCK1/PTEN/PI3K/Akt/VEGF pathway in vitro. Arctiin attenuates high glucose‐induced human retinal capillary endothelial cell proliferation by regulating ROCK1/PTEN/PI3K/Akt/VEGF pathway in vitro

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.15232

    Arctiin attenuates HG‐induced expression of VEGF and perturbation of the ROCK1/PTEN/PI3K/Akt signalling pathway in HRCECs. (A‐C) HRCECs were treated with HG (4.5 mg/mL) in the presence or absence of different concentrations of arctiin and then were characterized by Western blot to assess the expression of VEGFR2 and p‐VEGFR2. β‐actin served as the loading control, and the relative quantification of proteins was analysed by Adobe Photoshop software. (D) The expression level of VEGF‐A by ELISA Kit assay. (E‐L) HRCECs were treated as indicated in (A), and Western blot analysis was used to assess the expression of PI3K, p‐PI3K, Akt, p‐Akt, ROCK1 and PTEN. β‐actin served as the loading control, and the relative quantification of proteins was analysed by Adobe Photoshop software. All data are presented as the mean ± SD (* P
    Figure Legend Snippet: Arctiin attenuates HG‐induced expression of VEGF and perturbation of the ROCK1/PTEN/PI3K/Akt signalling pathway in HRCECs. (A‐C) HRCECs were treated with HG (4.5 mg/mL) in the presence or absence of different concentrations of arctiin and then were characterized by Western blot to assess the expression of VEGFR2 and p‐VEGFR2. β‐actin served as the loading control, and the relative quantification of proteins was analysed by Adobe Photoshop software. (D) The expression level of VEGF‐A by ELISA Kit assay. (E‐L) HRCECs were treated as indicated in (A), and Western blot analysis was used to assess the expression of PI3K, p‐PI3K, Akt, p‐Akt, ROCK1 and PTEN. β‐actin served as the loading control, and the relative quantification of proteins was analysed by Adobe Photoshop software. All data are presented as the mean ± SD (* P

    Techniques Used: Expressing, Western Blot, Software, Enzyme-linked Immunosorbent Assay

    ROCK1 inhibitor Y‐27632 reverses PTEN activation, PI3K/Akt de‐phosphorylation and VEGF down‐regulation mediated by arctiin. (A‐H) HRCECs were pretreated with Y‐27632 (20 μmol/L) for 2 h, followed by treatment with arctiin for 48 h. Western blot was used to assess the expression of ROCK1, PTEN, PI3K, p‐PI3K, Akt and p‐Akt. β‐actin served as the loading control, and the relative quantification of proteins was analysed by Adobe Photoshop software.. (I) HRCECs were pretreated with Y‐27632 (20 μmol/L) for 2 h, followed by treatment with arctiin for 48 h. The cells supernatant were characterized by ELISA Kit assay. (J‐L) HRCECs were treated in (A), and Western blot was used to assess the expression of VEGFR2 and p‐VEGFR2. β‐actin served as the loading control, and the relative quantification of proteins was analysed by Adobe Photoshop software. All data are presented as the mean ± SD (* P
    Figure Legend Snippet: ROCK1 inhibitor Y‐27632 reverses PTEN activation, PI3K/Akt de‐phosphorylation and VEGF down‐regulation mediated by arctiin. (A‐H) HRCECs were pretreated with Y‐27632 (20 μmol/L) for 2 h, followed by treatment with arctiin for 48 h. Western blot was used to assess the expression of ROCK1, PTEN, PI3K, p‐PI3K, Akt and p‐Akt. β‐actin served as the loading control, and the relative quantification of proteins was analysed by Adobe Photoshop software.. (I) HRCECs were pretreated with Y‐27632 (20 μmol/L) for 2 h, followed by treatment with arctiin for 48 h. The cells supernatant were characterized by ELISA Kit assay. (J‐L) HRCECs were treated in (A), and Western blot was used to assess the expression of VEGFR2 and p‐VEGFR2. β‐actin served as the loading control, and the relative quantification of proteins was analysed by Adobe Photoshop software. All data are presented as the mean ± SD (* P

    Techniques Used: Activation Assay, De-Phosphorylation Assay, Western Blot, Expressing, Software, Enzyme-linked Immunosorbent Assay

    38) Product Images from "Necroptosis is a key mediator of enterocytes loss in intestinal ischaemia/reperfusion injury"

    Article Title: Necroptosis is a key mediator of enterocytes loss in intestinal ischaemia/reperfusion injury

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.12987

    Necrostatin‐1 inhibits OGD ‐induced HMGB 1 translocation from the nucleus to the cytoplasm and HMGB 1 signalling activation. ( A ) Translocation of HMGB 1 (green) was detected in cells after OGD challenge. The nuclei were stained with Hoechst (blue, bar denotes 20 μm). White arrows indicate HMGB 1 translocation from the nucleus to the cytoplasm. ( B ) IEC ‐6 cytoplasmic and total extracts were analysed for HMGB 1 expression by Western blot. ( C ) Supernatants HMGB 1 levels were analysed by ELISA . ( D and E ) Western blot and quantification show the down‐regulated expression of RAGE and TLR 4 after Nec‐1 pre‐treatment. The data are shown as the means ± S.D. ( n = 6 per group). * P
    Figure Legend Snippet: Necrostatin‐1 inhibits OGD ‐induced HMGB 1 translocation from the nucleus to the cytoplasm and HMGB 1 signalling activation. ( A ) Translocation of HMGB 1 (green) was detected in cells after OGD challenge. The nuclei were stained with Hoechst (blue, bar denotes 20 μm). White arrows indicate HMGB 1 translocation from the nucleus to the cytoplasm. ( B ) IEC ‐6 cytoplasmic and total extracts were analysed for HMGB 1 expression by Western blot. ( C ) Supernatants HMGB 1 levels were analysed by ELISA . ( D and E ) Western blot and quantification show the down‐regulated expression of RAGE and TLR 4 after Nec‐1 pre‐treatment. The data are shown as the means ± S.D. ( n = 6 per group). * P

    Techniques Used: Translocation Assay, Activation Assay, Staining, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay

    Intestinal protection by necrostatin‐1 versus intestinal I/R injury in vivo . ( A ) Histopathologic changes in the intestinal mucosa. Haematoxylin and eosin stained small intestine after 1 hr ischaemia followed by 6 hrs/24 hrs of reperfusion. Magnification is ×200, bar denotes 100 mm. Black arrows indicate denuded, fused villi and haemorrhage. Black asterisks indicate Gruenhagen's space. ( B ) Injury scores of the intestinal mucosa morphology. ( C ) Intestinal cellular injury evaluated by serum DAO activity. ( D ) Serum HMGB 1 level were analysed by ELISA . The images are representative for each group. The data are shown as the means ± S.D. ( n = 8 per group). * P
    Figure Legend Snippet: Intestinal protection by necrostatin‐1 versus intestinal I/R injury in vivo . ( A ) Histopathologic changes in the intestinal mucosa. Haematoxylin and eosin stained small intestine after 1 hr ischaemia followed by 6 hrs/24 hrs of reperfusion. Magnification is ×200, bar denotes 100 mm. Black arrows indicate denuded, fused villi and haemorrhage. Black asterisks indicate Gruenhagen's space. ( B ) Injury scores of the intestinal mucosa morphology. ( C ) Intestinal cellular injury evaluated by serum DAO activity. ( D ) Serum HMGB 1 level were analysed by ELISA . The images are representative for each group. The data are shown as the means ± S.D. ( n = 8 per group). * P

    Techniques Used: In Vivo, Staining, Activity Assay, Enzyme-linked Immunosorbent Assay

    39) Product Images from "LncRNA ZNFTR functions as an inhibitor in pancreatic cancer by modulating ATF3/ZNF24/VEGFA pathway"

    Article Title: LncRNA ZNFTR functions as an inhibitor in pancreatic cancer by modulating ATF3/ZNF24/VEGFA pathway

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-021-04119-3

    VEGFA was regulated by ZNFTR via ZNF24. A After transfected with pcDNA-Vector or pcDNA-ZNF24, and siNC or siZNF24 #1/2 in PANC-1 cells, the expression of VEGFA both at mRNA and protein levels was detected by qRT-PCR and western blot, respectively. B After transfected with pcDNA-Vector or pcDNA-ZNF24, and siNC or siZNF24 #1/2 in PANC-1 cells, the VEGFA secretion level in supernatants was detected by ELISA assay. C ChIP assay analyzed the enrichment level of VEGFA promoter after co-transfected siZNFTR with or without pcDNA-ZNF24 in PANC-1 cells. D After transfected with a vector containing wild type (WT) or mutant binding site (MUT) of VEGFA promoter, the activity of the VEGFA promoter after co-transfected siZNFTR with or without pcDNA-ZNF24 was assessed via luciferase reporter assay in PANC-1 cells. E Left: Co-transfected siZNFTR with or without pcDNA-ZNF24, the expression of VEGFA was analyzed by qRT-PCR and western blot, respectively. Right: Co-transfected pcDNA-ZNFTR with or without siZNF24, the expression of VEGFA was analyzed by qRT-PCR and western blot, respectively. F After co-transfected siZNFTR with or without pcDNA-ZNF24, and co-transfected pcDNA-ZNFTR with or without siZNF24, VEGFA secretion level in supernatants was detected by ELISA assay. G Representative images and quantifications of the tube formation ability of HUVEC treated with different condition medium collected from transfected cells (co-transfected siZNFTR with or without pcDNA-ZNF24, co-transfected pcDNA-ZNFTR with or without siZNF24) was performed by tube formation assay. All data were revealed as means ± standard deviation (SD) for no less than three independent experiments. Significant P values showed as * P
    Figure Legend Snippet: VEGFA was regulated by ZNFTR via ZNF24. A After transfected with pcDNA-Vector or pcDNA-ZNF24, and siNC or siZNF24 #1/2 in PANC-1 cells, the expression of VEGFA both at mRNA and protein levels was detected by qRT-PCR and western blot, respectively. B After transfected with pcDNA-Vector or pcDNA-ZNF24, and siNC or siZNF24 #1/2 in PANC-1 cells, the VEGFA secretion level in supernatants was detected by ELISA assay. C ChIP assay analyzed the enrichment level of VEGFA promoter after co-transfected siZNFTR with or without pcDNA-ZNF24 in PANC-1 cells. D After transfected with a vector containing wild type (WT) or mutant binding site (MUT) of VEGFA promoter, the activity of the VEGFA promoter after co-transfected siZNFTR with or without pcDNA-ZNF24 was assessed via luciferase reporter assay in PANC-1 cells. E Left: Co-transfected siZNFTR with or without pcDNA-ZNF24, the expression of VEGFA was analyzed by qRT-PCR and western blot, respectively. Right: Co-transfected pcDNA-ZNFTR with or without siZNF24, the expression of VEGFA was analyzed by qRT-PCR and western blot, respectively. F After co-transfected siZNFTR with or without pcDNA-ZNF24, and co-transfected pcDNA-ZNFTR with or without siZNF24, VEGFA secretion level in supernatants was detected by ELISA assay. G Representative images and quantifications of the tube formation ability of HUVEC treated with different condition medium collected from transfected cells (co-transfected siZNFTR with or without pcDNA-ZNF24, co-transfected pcDNA-ZNFTR with or without siZNF24) was performed by tube formation assay. All data were revealed as means ± standard deviation (SD) for no less than three independent experiments. Significant P values showed as * P

    Techniques Used: Transfection, Plasmid Preparation, Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Chromatin Immunoprecipitation, Mutagenesis, Binding Assay, Activity Assay, Luciferase, Reporter Assay, Tube Formation Assay, Standard Deviation

    40) Product Images from "IL-33 Alleviates Postoperative Cognitive Impairment by Inhibiting Hippocampal Inflammation and Upregulating Excitatory Synaptic Number in Aged Mice"

    Article Title: IL-33 Alleviates Postoperative Cognitive Impairment by Inhibiting Hippocampal Inflammation and Upregulating Excitatory Synaptic Number in Aged Mice

    Journal: Brain Sciences

    doi: 10.3390/brainsci12091244

    IL-33 inhibits surgery/anesthesia-induced hippocampal inflammation in aged mice. Activation of microglia in the hippocampus was indicated by Iba1 ( A , B ). The levels of TNF-α ( C ), IL-1β ( D ) and IL-10 ( E ) were detected by ELISA 3 days after surgery. Data are expressed as the mean ± SD (one-way ANOVA followed by Bonferroni’s post hoc test, n = 4 per group). ** p
    Figure Legend Snippet: IL-33 inhibits surgery/anesthesia-induced hippocampal inflammation in aged mice. Activation of microglia in the hippocampus was indicated by Iba1 ( A , B ). The levels of TNF-α ( C ), IL-1β ( D ) and IL-10 ( E ) were detected by ELISA 3 days after surgery. Data are expressed as the mean ± SD (one-way ANOVA followed by Bonferroni’s post hoc test, n = 4 per group). ** p

    Techniques Used: Mouse Assay, Activation Assay, Enzyme-linked Immunosorbent Assay

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    Boster Bio apoa1
    The relationship between the concentrations of <t>APOA1</t> (R=0.426, p=0.043) and RBP4 (R=0.574, p=0.004) in the vitreous and the extent of retinal detachment in patients with RRDCD.
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    Boster Bio mouse cxcl1 kc picokine elisa kit
    MMP-2 and MMP-9 protein levels ( a , b ) and activities ( c , d ) in BALF and lung tissues. Mice were intratracheally instilled with 50 µg per mouse of Nano-Ni, or with either partially passivated (Nano-Ni–P) or carbon-coated (Nano-Ni–C) nickel nanoparticles with same molar concentration of Ni as Nano-Ni. Control mice were instilled with physiological saline. BALF and lung tissues were collected from mice at day 3 post-exposure. a , b MMP-2 and MMP-9 protein levels in the BALF determined by Mouse MMP-2 or MMP-9 <t>PicoKine™</t> <t>ELISA</t> Kit. Data are shown as mean ± SE (n = 5). * p
    Mouse Cxcl1 Kc Picokine Elisa Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Effects of VitD 3 on intestinal permeability and inflammatory cytokine secretion in serum of mice. (a) DAO activity in serum. (b) D-LA concentration in serum. (c) TNF- α concentration in serum. (d) IL-1 β concentration in serum. (e) IL-6 concentration in serum. (f) <t>IL-10</t> concentration in serum. All data were presented as mean ± SEM ( n = 10). ∗ P
    Mouse Il 10 Elisa Kit Picokine, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Sleep deprivation induced cognitive impairment. (A) The escape latency during 5 days of training and (B) The trajectory of the last experiment in a Morris water maze assay was used to measure the learning and memory ability. (C) The expression of inflammatory cytokines <t>(IL-6,</t> IL-1β, TNF-α) was detected by an <t>ELISA</t> assay kit. Data are mean ± SD of at least three duplicate experiments. * p
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    Image Search Results


    The relationship between the concentrations of APOA1 (R=0.426, p=0.043) and RBP4 (R=0.574, p=0.004) in the vitreous and the extent of retinal detachment in patients with RRDCD.

    Journal: Molecular Vision

    Article Title: Vitreous levels of apolipoprotein A1 and retinol binding protein 4 in human rhegmatogenous retinal detachment associated with choroidal detachment

    doi:

    Figure Lengend Snippet: The relationship between the concentrations of APOA1 (R=0.426, p=0.043) and RBP4 (R=0.574, p=0.004) in the vitreous and the extent of retinal detachment in patients with RRDCD.

    Article Snippet: Liao et al. [ ] demonstrated via in vitro experiments that APOA1 was able to inhibit activated neutrophils from adhering to fibronectin, inhibit neutrophil oxidation, reduce neutrophil degranulation, as well as reduce neutrophil killing.

    Techniques:

    Scatter plots of concentration of APOA1 and RBP4. Scatter plots of concentrations of APOA1 ( A ) and RBP4 ( B ). The difference in the APOA1 and RBP4 concentrations between groups was statistically significant (p

    Journal: Molecular Vision

    Article Title: Vitreous levels of apolipoprotein A1 and retinol binding protein 4 in human rhegmatogenous retinal detachment associated with choroidal detachment

    doi:

    Figure Lengend Snippet: Scatter plots of concentration of APOA1 and RBP4. Scatter plots of concentrations of APOA1 ( A ) and RBP4 ( B ). The difference in the APOA1 and RBP4 concentrations between groups was statistically significant (p

    Article Snippet: Liao et al. [ ] demonstrated via in vitro experiments that APOA1 was able to inhibit activated neutrophils from adhering to fibronectin, inhibit neutrophil oxidation, reduce neutrophil degranulation, as well as reduce neutrophil killing.

    Techniques: Concentration Assay

    The relationship between the concentrations of APOA1 (R=0.426, p=0.024) and RBP4 (R=0.397, p=0.036) in the vitreous and the extent of retinal detachment in patients with RRD.

    Journal: Molecular Vision

    Article Title: Vitreous levels of apolipoprotein A1 and retinol binding protein 4 in human rhegmatogenous retinal detachment associated with choroidal detachment

    doi:

    Figure Lengend Snippet: The relationship between the concentrations of APOA1 (R=0.426, p=0.024) and RBP4 (R=0.397, p=0.036) in the vitreous and the extent of retinal detachment in patients with RRD.

    Article Snippet: Liao et al. [ ] demonstrated via in vitro experiments that APOA1 was able to inhibit activated neutrophils from adhering to fibronectin, inhibit neutrophil oxidation, reduce neutrophil degranulation, as well as reduce neutrophil killing.

    Techniques:

    Correlation between APOA1 and RBP4 in each group. APOA1/RBP4 (R=0.594, p=0.003) in the RRDCD group ( A ) and APOA1/RBP4 (R=0.708, p

    Journal: Molecular Vision

    Article Title: Vitreous levels of apolipoprotein A1 and retinol binding protein 4 in human rhegmatogenous retinal detachment associated with choroidal detachment

    doi:

    Figure Lengend Snippet: Correlation between APOA1 and RBP4 in each group. APOA1/RBP4 (R=0.594, p=0.003) in the RRDCD group ( A ) and APOA1/RBP4 (R=0.708, p

    Article Snippet: Liao et al. [ ] demonstrated via in vitro experiments that APOA1 was able to inhibit activated neutrophils from adhering to fibronectin, inhibit neutrophil oxidation, reduce neutrophil degranulation, as well as reduce neutrophil killing.

    Techniques:

    MMP-2 and MMP-9 protein levels ( a , b ) and activities ( c , d ) in BALF and lung tissues. Mice were intratracheally instilled with 50 µg per mouse of Nano-Ni, or with either partially passivated (Nano-Ni–P) or carbon-coated (Nano-Ni–C) nickel nanoparticles with same molar concentration of Ni as Nano-Ni. Control mice were instilled with physiological saline. BALF and lung tissues were collected from mice at day 3 post-exposure. a , b MMP-2 and MMP-9 protein levels in the BALF determined by Mouse MMP-2 or MMP-9 PicoKine™ ELISA Kit. Data are shown as mean ± SE (n = 5). * p

    Journal: Journal of Nanobiotechnology

    Article Title: Comparative mouse lung injury by nickel nanoparticles with differential surface modification

    doi: 10.1186/s12951-018-0436-0

    Figure Lengend Snippet: MMP-2 and MMP-9 protein levels ( a , b ) and activities ( c , d ) in BALF and lung tissues. Mice were intratracheally instilled with 50 µg per mouse of Nano-Ni, or with either partially passivated (Nano-Ni–P) or carbon-coated (Nano-Ni–C) nickel nanoparticles with same molar concentration of Ni as Nano-Ni. Control mice were instilled with physiological saline. BALF and lung tissues were collected from mice at day 3 post-exposure. a , b MMP-2 and MMP-9 protein levels in the BALF determined by Mouse MMP-2 or MMP-9 PicoKine™ ELISA Kit. Data are shown as mean ± SE (n = 5). * p

    Article Snippet: The level of CXCL1/KC was assessed by a Mouse CXCL1/KC PicoKine™ ELISA Kit (Boster Biological, Pleasanton, CA, USA).

    Techniques: Mouse Assay, Concentration Assay, Enzyme-linked Immunosorbent Assay

    Effects of VitD 3 on intestinal permeability and inflammatory cytokine secretion in serum of mice. (a) DAO activity in serum. (b) D-LA concentration in serum. (c) TNF- α concentration in serum. (d) IL-1 β concentration in serum. (e) IL-6 concentration in serum. (f) IL-10 concentration in serum. All data were presented as mean ± SEM ( n = 10). ∗ P

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Vitamin D3 Protects Mice from Diquat-Induced Oxidative Stress through the NF-κB/Nrf2/HO-1 Signaling Pathway

    doi: 10.1155/2021/6776956

    Figure Lengend Snippet: Effects of VitD 3 on intestinal permeability and inflammatory cytokine secretion in serum of mice. (a) DAO activity in serum. (b) D-LA concentration in serum. (c) TNF- α concentration in serum. (d) IL-1 β concentration in serum. (e) IL-6 concentration in serum. (f) IL-10 concentration in serum. All data were presented as mean ± SEM ( n = 10). ∗ P

    Article Snippet: The kits to detect the concentration of TNF-α (Catalog number EK0527), IL-1β (Catalog number EK0394), IL-6 (Catalog number EK0411), and IL-10 (Catalog number EK0417) in serum were purchased from Boster (Wuhan, China).

    Techniques: Permeability, Mouse Assay, Activity Assay, Concentration Assay

    Sleep deprivation induced cognitive impairment. (A) The escape latency during 5 days of training and (B) The trajectory of the last experiment in a Morris water maze assay was used to measure the learning and memory ability. (C) The expression of inflammatory cytokines (IL-6, IL-1β, TNF-α) was detected by an ELISA assay kit. Data are mean ± SD of at least three duplicate experiments. * p

    Journal: Frontiers in Neurology

    Article Title: Sleep Deprivation Induces Cognitive Impairment by Increasing Blood-Brain Barrier Permeability via CD44

    doi: 10.3389/fneur.2020.563916

    Figure Lengend Snippet: Sleep deprivation induced cognitive impairment. (A) The escape latency during 5 days of training and (B) The trajectory of the last experiment in a Morris water maze assay was used to measure the learning and memory ability. (C) The expression of inflammatory cytokines (IL-6, IL-1β, TNF-α) was detected by an ELISA assay kit. Data are mean ± SD of at least three duplicate experiments. * p

    Article Snippet: IL-6 (EK0411, Boster Biological Technology Co. Ltd), IL-1β (EK0394, Boster Biological Technology Co. Ltd), and tumor necrosis factor (TNF)-α (EK0527, Boster Biological Technology Co. Ltd) ELISA kits were used to measure the levels of IL-6, IL-1β, and TNF-α in the mouse hippocampus tissue following the instructions from the manufacturer.

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay