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2009•Wuhan Daxue xuebao. Yixue banRequires access

Effects of Hydrogen Sulfide on Cardiomyocytes Apoptosis Induced by Oxidative Injury

XU Zeng-guang

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Abstract

Objective: To investigate the effect of H2S on apoptosis induced by oxidative injury in cardiomyocytes.Methods: Neonatal rat cardiomyocytes were treated with 0.1 mmol/L H2O2 to establish the oxidative stress damage moded.Then the cell viability,lactate dehydrogenase(LDH) and malondialdehyde(MDA) content were measured to evaluate the effect of H2S on apoptosis induced by oxidative injury.Besides,the cell apoptosis was detected by double-staining(Annexin V-FITC/PI).Results: H2O2 was able to induce apoptosis in cardiomyocytes markedly.H2S treatment significantly decreased LDH leakage and MDA production,and various concentration of H2S pretreatment could decrease the apoptosis rate significantly.Conclusion: Pretreatment with H2S protects cardiomyocytes from oxidative injury through inhibiting apoptosis induced by H2O2 and this anti-apoptotic effect is dose-dependent in a certain range.

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Objective: To investigate the effect of H2S on apoptosis induced by oxidative injury in cardiomyocytes.Methods: Neonatal rat cardiomyocytes were treated with 0.1 mmol/L H2O2 to establish the oxidative stress damage moded.Then the cell viability,lactate dehydrogenase(LDH) and malondialdehyde(MDA) content were measured to evaluate the effect of H2S on apoptosis induced by oxidative injury.Besides,the cell apoptosis was detected by double-staining(Annexin V-FITC/PI).Results: H2O2 was able to induce apoptosis in cardiomyocytes markedly.H2S treatment significantly decreased LDH leakage and MDA production,and various concentration of H2S pretreatment could decrease the apoptosis rate significantly.Conclusion: Pretreatment with H2S protects cardiomyocytes from oxidative injury through inhibiting apoptosis induced by H2O2 and this anti-apoptotic effect is dose-dependent in a certain range.

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Available abstract

Objective: To investigate the effect of H2S on apoptosis induced by oxidative injury in cardiomyocytes.Methods: Neonatal rat cardiomyocytes were treated with 0.1 mmol/L H2O2 to establish the oxidative stress damage moded.Then the cell viability,lactate dehydrogenase(LDH) and malondialdehyde(MDA) content were measured to evaluate the effect of H2S on apoptosis induced by oxidative injury.Besides,the cell apoptosis was detected by double-staining(Annexin V-FITC/PI).Results: H2O2 was able to induce apoptosis in cardiomyocytes markedly.H2S treatment significantly decreased LDH leakage and MDA production,and various concentration of H2S pretreatment could decrease the apoptosis rate significantly.Conclusion: Pretreatment with H2S protects cardiomyocytes from oxidative injury through inhibiting apoptosis induced by H2O2 and this anti-apoptotic effect is dose-dependent in a certain range.

Key concepts: Apoptosis, Malondialdehyde, Annexin, Lactate dehydrogenase, Oxidative stress, Chemistry, Viability assay, Oxidative phosphorylation

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