1. Ginsenoside Rb1 Inhibits Cardiomyocyte Autophagy via PI3K/Akt/mTOR Signaling Pathway and Reduces Myocardial Ischemia/Reperfusion Injury.
- Author
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Qin, Guo-Wei, Lu, Pan, Peng, Li, and Jiang, Wei
- Subjects
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FLOW cytometry , *INTERLEUKINS , *IN vitro studies , *BIOLOGICAL models , *MYOCARDIUM , *HEART cells , *STAINS & staining (Microscopy) , *AUTOPHAGY , *MYOCARDIAL ischemia , *ANIMAL experimentation , *WESTERN immunoblotting , *IMMUNOHISTOCHEMISTRY , *ONE-way analysis of variance , *GLYCOSIDES , *MYOCARDIAL infarction , *APOPTOSIS , *CELLULAR signal transduction , *MYOCARDIAL reperfusion complications , *GENE expression , *T-test (Statistics) , *TUMOR necrosis factors , *ENZYME-linked immunosorbent assay , *DESCRIPTIVE statistics , *RESEARCH funding , *DATA analysis software , *CELL lines , *MICE , *HYPOXEMIA - Abstract
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 β , TNF- α 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. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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