Benzoylaconine improves mitochondrial function in oxygenglucose deprivation and reperfusion-induced cardiomyocyte injury by activation of the AMPK/PGC-1 axis
10.4196/kjpp.2022.26.5.325
- Author:
Leijie CHEN
1
;
Laixing YAN
;
Weiwei ZHANG
Author Information
1. Department of Cardiology, Hebi People’s Hospital, Hebi 458030, China
- Publication Type:Original Article
- From:The Korean Journal of Physiology and Pharmacology
2022;26(5):325-333
- CountryRepublic of Korea
- Language:English
-
Abstract:
Heart failure (HF) has become one of the severe public health problems.The detailed role of mitochondrial function in HF was still unclear. Benzoylaconine (BAC) is a traditional Chinese medicine, but its role in HF still needs to be explored.In this study, oxygen-glucose deprivation and reperfusion (OGD/R) was executed to mimic the injury of H9C2 cells in HF. The viability of H9C2 cells was assessed via MTT assay. OGD/R treatment markedly decreased the viability of H9C2 cells, but BAC treatment evidently increased the viability of OGD/R-treated H9C2 cells. The apoptosis of H9C2 was enhanced by OGD/R treatment but suppressed by BAC treatment. The mitochondrial membrane potential was evaluated via JC-1 assay. BAC improved the mitochondrial function and suppressed oxidative stress in OGD/R-treated H9C2 cells. Moreover, Western blot analysis revealed that the protein expression of p-AMPK and PGC-1α were reduced in OGD/R-treated H9C2 cells, which was reversed by BAC. Rescue assays indicated that AMPK attenuation reversed the BAC-mediated protective effect on OGD/R-treated cardiomyocytes. Moreover, BAC alleviated myocardial injury in vivo. In a word, BAC modulated the mitochondrial function in OGD/R-induced cardiomyocyte injury by activation of the AMPK/PGC-1 axis. The findings might provide support for the application of BAC in the treatment of HF.
