The effect of activating retinoid X receptor inhibiting hydrogen peroxide-induced apoptosis in cultured rat neonatal cardiomyocytes
- VernacularTitle:激动维甲类X受体抑制过氧化氢诱导的心肌细胞凋亡
- Author:
Peiren SHAN
;
Ancai YUAN
;
Limin WANG
;
Linghong SHEN
;
Dajun CHAI
;
Lei ZHOU
;
Jun PU
;
Ben HE
- Publication Type:Journal Article
- Keywords:
Retinoid X receptor;
Cardiomyoeytes;
Apoptosis;
Oxidative stress
- From:
Chinese Journal of Emergency Medicine
2008;17(5):464-468
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of 9-cis retinoid acid(c-RA),a retinoid X receptor(RXR)agonist,on hydrogen peroxide(H2O2)induced apoptosis in cultured rat neonatal cardiomyoeytes,and to explore the mechanism.Method Cultured cardiomyocpes were randomly divided into three groups:normal group treated with vehicle(N group),H2O2 group treated with 100 μmol/L H2O2(H group),and c-RA group pretreated with 100nmol/L c-RA(H+R group).Cell viability was detected by MTT.Morphological changes of apoptotic cardiomyocytes were observed by Hoechst 33258 staining under fluorescence microscope.The apoptotic rate was determined by flow cytometry.Mitochondrial membrane potential(△(ψ)m)was measured by JC-1 dye.Cellular reactive oxygen species(ROS)production was detected by CM-H2DCFDA fluorescent probe.All measurement data wIe expressed as(x±s),and statistically analyzed using one-way ANOVA analysis and Dunnett test.Differences were considered significant when P was＜0.05.Results Treatment with c-RA significantly enhanced cell viability,reduced apoptosis ratio,stabled mitoehondrial membrane potential and reduced level of cellular reactive oxygen species.Conclusions RXR agonist c-RA inhibits H2O2-induced myocyte apoptosis in cultured rat neonatal cardiomyocytes,which may be related to alleviate oxidative stress injury.
