2012Zhongguo shengwu huaxue yu fenzi shengwu xuebaoRequires access

Protection of α-Lipoic Acid Against H_2O_2-induced Oxidative Stress in H9c2 Cells

Liu Yi

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Abstract

The oxygen free radicals produced by cardiac ischemia/reperfusion injury can cause cardiomyocyte apoptosis.α-Lipoic acid(LA) plays a role in anti-oxidation.However,whether LA has cytoprotective potential to protect cardiomyocytes from apoptosis remains unclear.In this study,H2O2-induced injury in H9c2 cells was used as a cell model,the anti-apoptosis potential of LA against oxidative injury was evaluated by CCK-8 determination for cell viability,by Hoechst33342 staining for nucleus morphology,by flow cytometry assay for apoptosis rate,by real-time PCR assessment for anti-apoptosis Bcl-2 and pro-apoptosis Bax gene expression.We found that LA could increase the cell survival of H2O2-induced injury in H9c2 cells and prevent H9c2 cells from oxidative stress-induced apoptosis.Furthermore,LA mediated the anti-apoptosis role by upregulating Bcl-2 expression.The results suggest that LA may have protective effect for the H2O2-induced apoptosis in H9c2 cells.These findings will contribute to the treatment of cardiomyocyte apoptosis induced by oxidative stress.

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What this paper is about

The oxygen free radicals produced by cardiac ischemia/reperfusion injury can cause cardiomyocyte apoptosis.α-Lipoic acid(LA) plays a role in anti-oxidation.However,whether LA has cytoprotective potential to protect cardiomyocytes from apoptosis remains unclear.In this study,H2O2-induced injury in H9c2 cells was used as a cell model,the anti-apoptosis potential of LA against oxidative injury was evaluated by CCK-8 determination for cell viability,by Hoechst33342 staining for nucleus morphology,by flow cytometry assay for apoptosis rate,by real-time PCR assessment for anti-apoptosis Bcl-2 and pro-apoptosis Bax gene expression.We found that LA could increase the cell survival of H2O2-induced injury in H9c2 cells and prevent H9c2 cells from oxidative stress-induced apoptosis.Furthermore,LA mediated the anti-apoptosis role by upregulating Bcl-2 expression.The results suggest that LA may have protective effect for the H2O2-induced apoptosis in H9c2 cells.These findings will contribute to the treatment of cardiomyocyte apoptosis induced by oxidative stress.

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Available abstract

The oxygen free radicals produced by cardiac ischemia/reperfusion injury can cause cardiomyocyte apoptosis.α-Lipoic acid(LA) plays a role in anti-oxidation.However,whether LA has cytoprotective potential to protect cardiomyocytes from apoptosis remains unclear.In this study,H2O2-induced injury in H9c2 cells was used as a cell model,the anti-apoptosis potential of LA against oxidative injury was evaluated by CCK-8 determination for cell viability,by Hoechst33342 staining for nucleus morphology,by flow cytometry assay for apoptosis rate,by real-time PCR assessment for anti-apoptosis Bcl-2 and pro-apoptosis Bax gene expression.We found that LA could increase the cell survival of H2O2-induced injury in H9c2 cells and prevent H9c2 cells from oxidative stress-induced apoptosis.Furthermore,LA mediated the anti-apoptosis role by upregulating Bcl-2 expression.The results suggest that LA may have protective effect for the H2O2-induced apoptosis in H9c2 cells.These findings will contribute to the treatment of cardiomyocyte apoptosis induced by oxidative stress.

Key concepts: Apoptosis, Oxidative stress, Flow cytometry, Viability assay, Cell biology, Chemistry, Reactive oxygen species, Cell

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