Protective role of STVNa in myocardial ischemia reperfusion injury by inhibiting mitochondrial fission
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Xiaoou Sun1, Yingying Yang2, Yanxiang Xie2, Xingjuan Shi3, Lijie Huang2 and Wen Tan1
1Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou 510006, China
2School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China
3Key Laboratory of Developmental Genes and Human Disease, Institute of Life Sciences, Southeast University, Nanjing 210096, China
Wen Tan, email: firstname.lastname@example.org
Keywords: STVNa; mitochondrial; ischemia reperfusion injury; cardioprotective
Received: May 30, 2017 Accepted: November 14, 2017 Published: December 05, 2017
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.
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