期刊
GENE
卷 808, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.gene.2021.145968
关键词
Myocardial ischemia-reperfusion; Resveratrol; Ferroptosis; Autophagy; Ubiquitination
资金
- Hunan Provincial Education Department Project [2014C0981]
- Scientific Research Projects of Health and Family Planning Commission in Hunan Province of China [B20180057]
- Xiangcai Education Project [2020SK51824]
Res has been shown to protect against myocardial I/R injury by reducing oxidative stress and inhibiting ferroptosis, potentially through the regulation of USP19-Beclin1 autophagy.
Resveratrol (Res) is a polyphenol with a variety of biological activities. However, whether Res can prevent myocardial ischemia-reperfusion (I/R) injury is not yet known. This study aimed to investigate the protective effect of Res on myocardial I/R injury and to explore its potential mechanism. H9c2 cells were used for the in vitro experiments and oxygen-glucose deprivation/reoxygenation (OGD/R) model was established. Rats were ligated and perfused by the left anterior descending branch with or without Res (50 mg/kg.bw) for 14 days.The higher level of oxidative stress and Fe2+ content was observed in OGD/R-induced H9c2 cells than that of normal cells. OGD/R-induced H9c2 cells showed increased ferroptosis, mainly by reducing the expression of glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1), but enhancing the expression of transferrin receptor 1 (TfR1). Both in vivo and in vitro experiments indicated that Res reduced the level of oxidative stress and Fe2+ content. In addition, Res inhibited ferroptosis, decreased TfR1 expression, and increased the expressions of FTH1 and GPX4 in OGD/R-induced H9c2 cells and I/R rats. Moreover, we found that Res inhibited ferroptosis by the regulation of ubiquity specific peptidase 19 (USP19)-Beclin1 autophagy. Res protects against myocardial I/R injury via reducing oxidative stress and attenuating fermptosis. Res could be a potential agent to the prevention of myocardial I/R injury.
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