期刊
AMERICAN JOURNAL OF CHINESE MEDICINE
卷 49, 期 8, 页码 1913-1927出版社
WORLD SCIENTIFIC PUBL CO PTE LTD
DOI: 10.1142/S0192415X21500907
关键词
Myocardial Ischemia; Reperfusion Injury; Ginsenoside Rb1; Autophagy; Hypoxia/Reoxygenation; PI3K; Akt; mTOR Pathway
资金
- Natural Science Foundation of Guangxi [2018GXNSFAA050110]
The study found that Ginsenoside Rb1 alleviated MIRI in rats and protected H9C2 cells against hypoxia/reoxygenation-induced damage. Ginsenoside Rb1 inhibited the autophagy process induced by MIRI, exerted protective effects through the PI3K/Akt/mTOR signaling pathway, and contributed to reducing cardiomyocyte apoptosis.
Myocardial ischemia/reperfusion injury (MIRI) is the major cause of myocardial cell damage in acute myocardial infarction, and its treatment remains a clinical challenge. Ginsenoside Rb1 showed protective effects on the cardiovascular system; however, the underlying mechanism remains largely unclear. Effects of Ginsenoside Rb1 on rat MIRI-induced myocardial infarct size were evaluated through TTC staining. TUNEL assay and flow cytometry analysis were employed to estimate cell apoptosis. Apoptosis, autophagy and PI3K/Akt/mTOR pathway-related proteins were estimated via western blot. Expression of Beclin1 in myocardial tissues were examined by immunohistochemical analysis. Expression levels of IL-1 beta, TNF-alpha and IL-6 were tested by enzyme-linked immunosorbent assay (ELISA). Here, we found that Ginsenoside Rb1 treatment not only alleviated MIRI in rats but also protected H9C2 cells against hypoxia/reoxygenation induced damage. Ginsenoside Rb1 abolished the MIRI-induced activation of autophagy. Meanwhile, we found that treatment of 3-MA (autophagy inhibitor) could enhance the protective effects of Ginsenoside Rb1 on H9C2 cells during H/R. Moreover, Ginsenoside Rb1 treatment resulted in the activation of the PI3K/Akt/mTOR pathway, and treatment of LY294002 (PI3K/Akt pathway repressor) abolished the protective effects of Ginsenoside Rb1 on myocardial in vitro and in vivo. Our results suggest that Ginsenoside Rb1 functions as a protector against MIRI by repressing cardiomyocyte autophagy through the PI3K/Akt/mTOR signaling pathway.
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