STVNa通过抑制线粒体分裂在心肌缺血再灌注损伤中的保护作用。

Protective role of STVNa in myocardial ischemia reperfusion injury by inhibiting mitochondrial fission.

作者信息

Sun Xiaoou, Yang Yingying, Xie Yanxiang, Shi Xingjuan, Huang Lijie, Tan Wen

机构信息

Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou 510006, China.

School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China.

出版信息

Oncotarget. 2017 Dec 5;9(2):1898-1905. doi: 10.18632/oncotarget.22969. eCollection 2018 Jan 5.

It has been reported that isosteviol, a widely known sweeteners, can protect against myocardial ischemia-reperfusion (IR) injury in isolated guinea pig heart. Here, we aim to confirm the cardioprotective effect of its sodium salt, isosteviol sodium (STVNa), against IR injury and its potential molecular mechanism in H9c2 cardiomyocytes. STVNa significantly improved cell viability, restored mitochondrial membrane potential, decreased cellular reactive oxygen species generation, and inhibited cell apoptosis. Furthermore, STVNa treatment changed the morphology of mitochondria from fragmented, discontinuous forms to normal elongated, tubular forms. Cyto-immunofluorescence and western blot analysis revealed that STVNa inhibited mitochondrial fission proteins dynamin-related protein 1 (Drp1), and mitochondrial fission 1 (Fis1), thus plays a key role in cardioprotection. These findings, for the first time, suggest that STVNa can protect against myocardial IR injury through reverse mitochondrial fission.

据报道，异甜菊醇作为一种广为人知的甜味剂，可保护离体豚鼠心脏免受心肌缺血再灌注（IR）损伤。在此，我们旨在证实其钠盐异甜菊醇钠（STVNa）对H9c2心肌细胞IR损伤的心脏保护作用及其潜在分子机制。STVNa显著提高细胞活力，恢复线粒体膜电位，减少细胞活性氧生成，并抑制细胞凋亡。此外，STVNa处理使线粒体形态从碎片化、不连续形式转变为正常的细长管状形式。细胞免疫荧光和蛋白质印迹分析表明，STVNa抑制线粒体分裂蛋白动力相关蛋白1（Drp1）和线粒体分裂蛋白1（Fis1），从而在心脏保护中起关键作用。这些发现首次表明，STVNa可通过逆转线粒体分裂来保护心肌免受IR损伤。