MFN1介导的线粒体融合在心肌细胞凋亡中的作用研究

Effect of MFN1 Mediated Mitochondrial Fusion on the Apoptosis of H9C2 Cardiomyocytes

目的:探讨线粒体融合关键蛋白MFN1介导的线粒体融合在调控心肌细胞凋亡中的作用。方法:通过si RNA降低体外培养H9C2心肌细胞中MFN1的表达后,采用Western blot检测线粒体细胞色素c(Cyto c)释放及其下游凋亡效应分子Caspase9与Caspase3活性,流式细胞术检测细胞内活性氧(ROS)的产生情况,流式细胞术检测细胞凋亡的情况。结果:干扰MFN1可显著促进H9C2心肌细胞内细胞色素c由线粒体释放至胞浆,促进Caspase9与Caspase3的激活,增加细胞内活性氧ROS产生并提高细胞凋亡率(均P<0.05)。结论:MFN1介导的线粒体融合可保护心肌细胞凋亡,其机制可能与抑制ROS产生与细胞色素C释放有关。

Objective： To investigate the role of MFN1-mediated mitochondrial fusion in the regulation of cardiomyocyte apoptosis.Methods： After knocking down of MFN1 with si RNA in H9 C2 cardiomyocytes, cytochrome c release, caspase9 and caspase3 activation,intracellular ROS and cell apoptosis were evaluated by western blotting and flow cytometry. Results： 1）. MFN1 significantly promoted the release of cytochrome cfrom the mitochondria to the cytosol, activation of caspase9 and caspase3 ROS production and apoptosis of H9 C2 cardiomyocytes（all P〈0.05）. Conclusion： MFN1-mediated mitochondrial fusion protects cardiomyocyte from apoptosis, which could be partially explained by the inhibition of ROS production and cytochrome c release.