缺血
再灌注损伤
药理学
医学
人参皂甙
心肌保护
人参
心脏病学
病理
替代医学
作者
Jian Ye,Tian-Jiao Lyu,Lingyan Li,Ying Liu,Hong Zhang,Xu Wang,Xin Xi,Zongjun Liu,Junqing Gao
出处
期刊:Phytomedicine
[Elsevier]
日期:2023-01-30
卷期号:113: 154681-154681
被引量:29
标识
DOI:10.1016/j.phymed.2023.154681
摘要
Ginsenoside Re is an active component in ginseng that confers protection against myocardial ischemia/reperfusion (I/R) injury. Ferroptosis is a type of regulated cell death found in various diseases.Our study aims to investigate the role of ferroptosis and the protective mechanism of Ginsenoside Re in myocardial ischemia/reperfusion.In the present study, we treated rats for five days with Ginsenoside Re, then established the myocardial ischemia/reperfusion injury rat model to detect molecular implications in myocardial ischemia/reperfusion regulation and to determine the underlying mechanism.This study identifies the mechanism behind ginsenoside Re's effect on myocardial ischemia/reperfusion injury and its regulation of ferroptosis through miR-144-3p. Ginsenoside Re significantly reduced cardiac damage caused by ferroptosis during myocardial ischemia/reperfusion injury and glutathione decline. To determine how Ginsenoside Re regulated ferroptosis, we isolated exosomes from VEGFR2+ endothelial progenitor cells after ischemia/reperfusion injury and performed miRNA profiling to screen the miRNAs aberrantly expressed in the process of myocardial ischemia/reperfusion injury and ginsenoside Re treatment. We identified that miR-144-3p was upregulated in myocardial ischemia/reperfusion injury by luciferase report and qRT-PCR. We further confirmed that the solute carrier family 7 member 11 (SLC7A11) was the target gene of miR-144-3p by database analysis and western blot. In comparison with ferropstatin-1, a ferroptosis inhibitor, in vivo studies confirmed that ferropstatin-1 also diminished myocardial ischemia/reperfusion injury induced cardiac function damage.We demonstrated that ginsenoside Re attenuates myocardial ischemia/reperfusion induced ferroptosis via miR-144-3p/SLC7A11.
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