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caspase 3 activity assay kit  (Beyotime)
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Beyotime caspase 3 activity assay kit
Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS <t>production,</t> <t>caspase-3</t> activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
Caspase 3 Activity Assay Kit, supplied by Beyotime, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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caspase 3  (Novus Biologicals)
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Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS <t>production,</t> <t>caspase-3</t> activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
Caspase 3, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti cleaved caspase 3  (ABclonal Biotechnology)
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Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS <t>production,</t> <t>caspase-3</t> activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
Anti Cleaved Caspase 3, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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caspase 3 7 activity assay kit  (Elabscience Biotechnology)
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Elabscience Biotechnology caspase 3 7 activity assay kit
Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS <t>production,</t> <t>caspase-3</t> activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
Caspase 3 7 Activity Assay Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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caspase 3 7 activity assay kit - by Bioz Stars, 2026-10
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cleaved caspase 3  (Novus Biologicals)
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Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS <t>production,</t> <t>caspase-3</t> activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
Cleaved Caspase 3, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cleaved caspase 3  (ABclonal Biotechnology)
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Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS <t>production,</t> <t>caspase-3</t> activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
Cleaved Caspase 3, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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vegf  (ABclonal Biotechnology)
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Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS <t>production,</t> <t>caspase-3</t> activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
Vegf, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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caspase 3 activity assay kit  (Boster Bio)
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Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS <t>production,</t> <t>caspase-3</t> activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
Caspase 3 Activity Assay Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS production, caspase-3 activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet: Glibenclamide disrupted SUR1-PARP1 interaction to restore DNA repair and attenuate apoptosis and inflammation in HBE cells (A) Schematic diagram of HBE cells with different treatments, followed by RNA sequencing analysis. Groups: control, 20 ng/mL; TNF-α, 100 μmol/L; glibenclamide plus TNF-α. n = 2 per group. (B) Venn diagram of differentially expressed genes. (C) GO and KEGG enrichment analyses of 280 genes in the intersection shown in (B). (D) RT-qPCR analysis of HBE cells with different treatments as indicated. (E) Co-immunoprecipitation assay in HBE cells transfected with FLAG-SUR1 plasmids and treated with 20 ng/mL TNF-α or 100 μmol/L glibenclamide as indicated. L.E., long exposure. (F) HBE cells were treated as in (E), then subjected to cytoplasmic and nuclear protein fractionation followed by western blotting. Cyto, cytoplasm; Nu, nucleus. (G) Western blot analysis of HBE cells pretreated with 100 μmol/L glibenclamide for 30 min followed by TNF-α or LPS co-treatment for 1 h. (H–J) ROS production, caspase-3 activity, and apoptosis in HBE cells under indicated treatments. (K–M) HBE cells were pretreated with 100 μmol/L glibenclamide, 5 μmol/L olaparib, or their combination for 24 h, followed by 20 ng/mL TNF-α stimulation, and subjected to western blotting, caspase-3 activity assay, and apoptosis analysis by flow cytometry. Gli, glibenclamide. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. GO and KEGG enrichment analyses in (C) were performed using a hypergeometric test with false discovery rate (FDR) correction. Data in (D) and (G–M) were analyzed using one-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

Article Snippet: Caspase 3 Activity Assay Kit , Beyotime Biotechnology , Cat# C1115.

Techniques: RNA Sequencing, Analysis, Control, Quantitative RT-PCR, Co-Immunoprecipitation Assay, Transfection, Fractionation, Western Blot, Activity Assay, Caspase-3 Activity Assay, Flow Cytometry

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet:

Article Snippet: Caspase 3 Activity Assay Kit , Beyotime Biotechnology , Cat# C1115.

Techniques: Cell-Signaling, Recombinant, Transfection, Caspase-3 Activity Assay, Protein Extraction, Knock-Out, Sequencing, Control, Plasmid Preparation, Software, Analysis