外源性硫化氢对心肌肥大的保护作用

Protective effect of exogenous hydrogen sulfide on myocardial hypertrophy

目的：研究外源性硫化氢（H2S）对血管紧张素Ⅱ（AngⅡ）引起的心肌细胞肥大的保护作用。方法：将1～3日龄Wistar乳鼠心肌细胞培养48h，随机分为正常对照组、AngⅡ组、硫氢化钠组（NaHS组），其中AngⅡ组和NaHS组的心肌细胞经AngⅡ干预48h制备心肌肥大细胞模型，通过鬼笔环肽染色判定模型成功。NaHS组在肥大基础上用NaHS干预48h。JC-1染色观察各组线粒体膜电位势能变化。Mitosox测定各组活性氧（ROS）水平。Wester nblot检测心肌细胞相关蛋白表达水平。结果：AngⅡ能够建立大鼠心肌肥大细胞模型。对照组、NaHS组线粒体膜电位势能均明显高于AngⅡ组。NaHS组ROS、NADPH氧化酶（NOX）4水平均低于AngⅡ组。结论：H2S可减少心肌细胞线粒体氧化应激，减少心肌细胞凋亡。

Objective： To study the protective effect of hydrogen sulfide （H2S） on cardiac hypertrophy. Methods： Ventricular cardiomyocytes of Wistar neonatal rat （1 - 3 days old） were incubated for 48 h, then divided into control group, angiotension Ⅱ （Ang Ⅱ）group and sodium sulfide （NariS） group. Ventricular cardiomyocytes in Ang Ⅱ group and Naris group were treated with Ang Ⅱ as cell cardiac hypertrophy model, and evaluated by Phalloidin stain method. Cells in NariS group were treated with NariS for 48 h. Mitochondrial transmembrane potential in all groups were determined by JC-1. Reactive oxygen species（ROS） in mitochondria were measured by MitoSox Red. Relative protein was analyzed by Western blot. Results： Cell cardiac hypertrophy model could be successfully established by Ang Ⅱ treatment. Naris could significantly promote the formation of the cardiac myocyte myofibril myogenic section compared with the controls. Compared with Ang Ⅱ group, mitochondrial transmembrane potential in control and Naris groups were higher, whereas both ROS and nicotinamide adeninedinucleotide phosphate oxidase （NOX）4 in Naris group were decreased. Conclusion. H2S significantly reduces mitochondrial oxidative stress and cardiomyocyte apoptosis in cardiac hypertrophy.