Protective effect of epigallocatechin-3-gallate on hypoxia/reoxygenation injury in cardiac myocytes and its mechanism
10.3969/j.issn.1001-1978.2017.11.021
- VernacularTitle:表没食子儿茶素没食子酸酯对心肌细胞缺氧/复氧损伤的抑制作用及其机制
- Author:
jia Xiao ZHENG
1
;
Ting YU
;
Hua ZHANG
;
feng Chun LI
;
xia Ye CHEN
;
zhen Yong YANG
;
xin Chen LI
;
Jie JIAN
Author Information
1. 桂林医学院药学院
- Keywords:
EGCG;
H9c2 cardiac myocytes;
hypoxia/reoxygenation injury;
cell apoptosis;
PI3K/Akt;
caspase-3
- From:
Chinese Pharmacological Bulletin
2017;33(11):1584-1588
- CountryChina
- Language:Chinese
-
Abstract:
Aim To observe the protective effect of epigallocatechin-3-gallate (EGCG) on hypoxia/reoxygenation (H/R) injury of cardiac myocytes and its mechanisms.Methods H9c2 cardiac myocytes were cultured in vitro and randomly divided into five groups:normal group(N group),H/R group,EGCG low dose group (L group),EGCG medium dose group (M group),and EGCG high dose group(H group).The cardiomyocyte H/R injury model was established and EGCG was pretreated.Cell survival rate was tested by CCK-8 method.The cell apoptotic rate was detected using Annexin V-FITC/PI double staining.The contents of total antioxidant capacity(T-AOC) and tumor necrosis factor α(TNF-α) in cell culture medium were tested according to the kit instructions.The protein expression of Akt and p-Akt was observed using Western blot,while the gene expressions of PI3K,Akt,caspase3 were detected by using fluorescence quantitative PCR method.Results Compared with model group,EGCG increased cell survival rate and reduced the apoptosis after H/R injury.Meanwhile,pretreatment EGCG improved the activity of T-AOC,reduced the level of TNF-α,up-regulated the expression of PI3K,Akt and p-Akt,and down-regulated the expression of caspase3.Conclusion EGCG reduces apoptosis and protects cardiac myocytes by influencing PI3K/Akt signal path
