Ginsenoside Rb1 Inhibits Cardiomyocyte Autophagy via PI3K/Akt/mTOR Signaling Pathway and Reduces Myocardial Ischemia/Reperfusion Injury
| Autor: | Guo-Wei Qin, Jiang Wei, Peng Li, Lu Pan |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Ginsenosides
Apoptosis Myocardial Reperfusion Injury Pharmacology chemistry.chemical_compound Phosphatidylinositol 3-Kinases Western blot medicine Autophagy Animals LY294002 Myocytes Cardiac Protein kinase B PI3K/AKT/mTOR pathway TUNEL assay medicine.diagnostic_test TOR Serine-Threonine Kinases General Medicine medicine.disease eye diseases Rats Complementary and alternative medicine chemistry Reperfusion injury Proto-Oncogene Proteins c-akt Signal Transduction |
| Zdroj: | The American journal of Chinese medicine. 49(8) |
| ISSN: | 1793-6853 |
| Popis: | 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[Formula: see text], TNF-[Formula: see text] 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. |
| Databáze: | OpenAIRE |
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