Hydrogen sulfide protects H9c2 cardiomyoblasts against H2O2-induced apoptosis
Hydrogen sulfide protects H9c2 cardiomyoblasts against H2O2-induced apoptosis
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DOI：
10.1590/1414-431x20187626
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发表时间：
2019-04
影响因子：
2.3
通讯作者：
Y. Zhang;Guang-Qing Huang;Bing Wu;Xin Lin;W. Yang;Zunyu Ke;Jie Liu
中科院分区：
文献类型：
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作者：
Y. Zhang;Guang-Qing Huang;Bing Wu;Xin Lin;W. Yang;Zunyu Ke;Jie Liu
活性氧（reactive oxygen species，ROS）是一种高活性的化学物质，可引起不可逆的组织损伤，在心血管疾病中起重要作用。硫化氢（H2S）是一种气体递质，可作为ROS清除剂，具有心脏保护作用。在这项研究中，我们研究了H2S对H2 O2诱导的心肌细胞凋亡的细胞保护作用。在用H2 O2（100 μ M）攻击之前，用H2S（100 μ M）处理H9 c2大鼠心肌细胞24 h。然后通过膜联蛋白V和PI评估细胞凋亡，并使用荧光探针JC-1测量线粒体膜电位。我们的研究结果表明，硫化氢提高细胞活力，降低凋亡率，并保存线粒体膜电位。在H2 O2诱导的应激后用H2S处理的心肌细胞中也观察到Bcl-2与Bax的比率增加。我们的研究结果表明H2S在预防缺血/再灌注后心肌细胞死亡方面具有治疗潜力。
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.