Hydrogen sulfide protects H9c2 cardiomyoblasts against H2O2-induced apoptosis

Reactive oxygen species (ROS) are highly reactive chemical species that may cause irreversible tissue damage, and play a critical role in cardiovascular diseases. Hydrogen sulfide (H2S) is a gasotransmitter that acts as a ROS scavenger with cardio-protective effects. In this study, we investigated the cytoprotective effect of H2S against H2O2-induced apoptosis in cardiomyocytes. H9c2 rat cardiomyoblasts were treated with H2S (100 μM) 24 h before challenging with H2O2 (100 μM). Apoptosis was then assessed by annexin V and PI, and mitochondrial membrane potential was measured using a fluorescent probe, JC-1. Our results revealed that H2S improved cell viability, reduced the apoptotic rate, and preserved mitochondrial membrane potential. An increased Bcl-2 to Bax ratio was also seen in myocytes treated with H2S after H2O2-induced stress. Our findings indicated a therapeutic potential for H2S in preventing myocyte death following ischemia/reperfusion.活性氧（Reactive Oxygen Species, ROS）是一类具有高反应活性的化学物质，可造成不可逆的组织损伤，并在心血管疾病中发挥关键作用。硫化氢（Hydrogen Sulfide, H2S）是一种气体递质，可作为ROS清除剂，同时具备心脏保护功效。本研究探究了H2S对抗H₂O₂诱导的心肌细胞凋亡的细胞保护作用。实验中，我们先以100 μM浓度的H2S处理H9c2大鼠心肌成肌细胞，24小时后再用100 μM的H₂O₂进行刺激。随后通过膜联蛋白V（Annexin V）与碘化丙啶（Propidium Iodide, PI）双染法评估细胞凋亡情况，并使用荧光探针JC-1检测线粒体膜电位。实验结果显示，H2S可提升细胞活力、降低细胞凋亡率，并维持线粒体膜电位的完整性。经H₂O₂应激处理后，H2S处理组的心肌细胞中B细胞淋巴瘤-2（B-cell lymphoma-2, Bcl-2）与Bcl-2相关X蛋白（Bcl-2 associated X protein, Bax）的表达比值显著升高。本研究结果表明，H2S在预防缺血/再灌注引发的心肌细胞死亡方面具备治疗潜力。