Overexpression of heat-shock proteins B1 protected rat cardiac cell line H9c2 from H_2O_2-induced oxidative damage
- VernacularTitle:热休克蛋白B1对大鼠心肌细胞氧化应激性损伤的作用
- Author:
Li LIU
;
Su-Rong JIANG
;
Xiao-Jin ZHANG
;
Chen CHEN
;
Guo-Xian DING
;
Jun HUANG
;
Yunlin CHENG
;
- Publication Type:Journal Article
- Keywords:
Heat-shock proteins;
Mitochondria;
Oxidative Stress;
Myocardium
- From:
Chinese Journal of Geriatrics
2001;0(05):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To determine the effect of mitochondria on the protection of heat-shock proteins B1(HSPB1) from oxidative damage in rat cardiac cell.Methods HSPB1 gene-transfected rat cardiomyocytes cell line H9c2 (HSPB1 H9c2) and empty vector transfected H9c2 (control) were established,and treated by 0-1000?mol/L H_2O_2 for 2h.And then the cell morphology, mitochondrial membrane potential and endogenous reactive oxygen species (ROS) were detected. Results (1)HSPB1 inhibited the morphological changes induced by H_2O_2 markedly.(2)HSPB1 inhibited the loss of mitochondrial membrane potential induced by H_2O_2.Following the stimulation of 0,75,150,300,500,1000?mol/L H_2O_2,mitochondrial membrane potential in HSPB1 and control H9c2 cells were (10.0?0.11)vs (7.01?0.26),(9.11?0.17)vs (6.05?0.19),(7.69?0.28)vs (5.14?0.28),(6.95?0.13)vs (4.66?0.11),(6.61?0.20)vs (1.85?0.35),(6.60?0.05)vs (1.19?0.01),respectively (all P0.05).Conclusions HSPB1 protects rat cardiomyocytes cell line(H9c2) from oxidative damage,which suggests that stabilization of mitochondrial membrane potential and the decreased endogenous reactive oxygen species after oxidative stress may be involved in the protection of HSPB1 against oxidative stress in H9c2.
