1. Ginsenoside Rd Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Inflammation and Apoptosis through PI3K/Akt Signaling Pathway.
- Author
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Wang, Yuanping, Zheng, Jiading, Xiao, Xieyang, Feng, Cailing, Li, Yinghong, Su, Hui, Yuan, Ding, Wang, Qinghai, Huang, Peihong, and Jin, Lili
- Subjects
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INFLAMMATION prevention , *IN vitro studies , *MYOCARDIAL ischemia , *MYOCARDIAL reperfusion complications , *INTRAPERITONEAL injections , *PENTOBARBITAL , *STATISTICAL significance , *RESEARCH funding , *APOPTOSIS , *PHARMACEUTICAL chemistry , *ENZYME-linked immunosorbent assay , *CELLULAR signal transduction , *IN vivo studies , *REVERSE transcriptase polymerase chain reaction , *PLANT extracts , *MICE , *CELL culture , *IMMUNOHISTOCHEMISTRY , *GLYCOSIDES , *DRUG efficacy , *MYOCARDIUM , *MOLECULAR structure , *WESTERN immunoblotting , *ONE-way analysis of variance , *GINSENG , *PHOSPHOTRANSFERASES , *STAINS & staining (Microscopy) , *CELL survival , *HEALTH outcome assessment , *COMPARATIVE studies , *TIME , *ECHOCARDIOGRAPHY , *HEART cells , *TUMOR necrosis factors - Abstract
Myocardial ischemia/reperfusion (I/R) injury is the leading cause of death worldwide. Ginsenoside Rd (GRd) has cardioprotective properties but its efficacy and mechanism of action in myocardial I/R injury have not been clarified. This study investigated GRd as a potent therapeutic agent for myocardial I/R injury. Oxygen-glucose deprivation and reperfusion (OGD/R) and left anterior descending (LAD) coronary artery ligation were used to establish a myocardial I/R injury model in vitro and in vivo. In vivo, GRd significantly reduced the myocardial infarct size and markers of myocardial injury and improved the cardiac function in myocardial I/R injury mice. In vitro, GRd enhanced cell viability and protected the H9c2 rat cardiomyoblast cell line from OGD-induced injury GRd. The network pharmacology analysis predicted 48 potential targets of GRd for the treatment of myocardial I/R injury. GO and KEGG enrichment analysis indicated that the cardioprotective effects of GRd were closely related to inflammation and apoptosis mediated by the PI3K/Akt signaling pathway. Furthermore, GRd alleviated inflammation and cardiomyocyte apoptosis in vivo and inhibited OGD/R-induced apoptosis and inflammation in cardiomyocytes. GRd also increased PI3K and Akt phosphorylation, suggesting activation of the PI3K/Akt pathway, whereas LY294002, a PI3K inhibitor, blocked the GRd-induced inhibition of OGD/R-induced apoptosis and inflammation in H9c2 cells. The therapeutic effect of GRd in vivo and in vitro against myocardial I/R injury was primarily dependent on PI3K/Akt pathway activation to inhibit inflammation and cardiomyocyte apoptosis. This study provides new evidence for the use of GRd as a cardiovascular drug. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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