硫化氢对氧化损伤心肌细胞凋亡的影响

Effects of Hydrogen Sulfide on Cardiomyocytes Apoptosis Induced by Oxidative Injury

目的:观察硫化氢(H2S)对体外培养乳鼠心肌细胞氧化损伤所致凋亡的影响。方法:以0.1 mmol/LH2O2处理细胞建立心肌细胞氧化损伤的模型,检测不同浓度的H2S对氧化应激下细胞存活率乳酸脱氢酶(LDH)活性及丙二醛(MDA)含量的影响,Annexin V-FITC/PI双染色分析不同剂量的H2S对氧化应激所致心肌细胞凋亡的影响。结果:过氧化氢对心肌细胞有明显的损伤作用,H2S可使培养基中的LDH和MDA水平显著下降,不同剂量的H2S预处理均可显著降低H2O2诱导的凋亡。结论:H2S能有效对抗H2O2引起的氧化损伤,且对细胞凋亡有抑制作用,其抗凋亡效应在一定范围内呈剂量依赖关系。

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.