Protective effects of corosolic acid on doxorubicin-induced cardiotoxicity in H9c2 cardiomyocytes
10.3969/j.issn.1001-1528.2024.02.016
- VernacularTitle:科罗索酸对阿霉素诱导的H9c2心肌细胞的保护作用
- Author:
Xiang JIA
1
;
Wu-Bin HE
;
Qiu-Shi YANG
;
Jian-Hua HUANG
Author Information
1. 锦州医科大学附属第一医院, 辽宁 锦州 121000
- Keywords:
corosolic acid;
doxorubicin cardiotoxicity;
apoptosis;
ferroptosis;
reactive oxygen species;
Nrf2/GPX4 pathway
- From:
Chinese Traditional Patent Medicine
2024;46(2):451-457
- CountryChina
- Language:Chinese
-
Abstract:
AIM To investigate the protective effects and the mechanism of corosolic acid on doxorubicin-induced cardiotoxicity in H9c2 cardiomyocytes.METHODS To screen and determine the effective concentration of corosolic acid,the injury models of H9c2 cardiomyocytes established by 1 μmol/L doxorubicin were exposed to 24 h different concentrations of corosolic acid,followed by detections of their cell activity by MTT method;their cell apoptosis morphology by Hoechst 33342 staining method;their cell apoptosis rate by Annexin V-FITC/PI double staining method;their intracellular ROS level by DCFH-DA probe;their intracellular iron level by iron ion colorimetry;and their protein expressions of Bax,Bcl-2,cleaved-caspase3,Nrf2,GPX4 and Ptgs2 by Western blot.RESULTS Upon the doxorubicin-induced injury models of H9c2 cardiomyocytes,corosolic acid improved their viability and survival rate(P<0.05),decreased their levels of ROS and Fe2+ and the apoptosis rate(P<0.05),up-regulated the protein expressions of Bcl-2,Nrf2 and GPX4(P<0.05),and down-regulated the protein expressions of Bax,cleved-caspase 3 and Ptgs2(P<0.05).CONCLUSION Corosolic acid can inhibit the ROS level and apoptosis of doxorubicin-induced injury models of H9c2 cardiomyocytes,and the iron death as well via activating Nrf2/GPX4 pathway.
