Effect of estrogen on cardiac injury and cardiomyocyte apoptosis of rat induced by isoproterenol
10.3969/j.issn.1671-8348.2014.34.003
- VernacularTitle:雌激素对异丙肾上腺素诱导的大鼠心肌损伤及心肌细胞凋亡的影响
- Author:
Hongjun WANG
;
Jing MENG
- Publication Type:Journal Article
- Keywords:
estrogen;
isoproterenol;
cardiomyocyte inj ury;
apoptosis
- From:
Chongqing Medicine
2014;(34):4566-4569,4573
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of estrogen on cardiac injury and cardiomyocyte apoptosis of rat induced by isoprotere-nol by modeling cardiac inj ury induced by bilateral ovariectomized (OVX)and isoproterenol (ISO).Methods Fifty female SD rats with bilateral ovariectomy and sham operation (Sham)were randomly divided into 5 groups:sham operation group (Sham group), bilateral ovariectomy group (OVX group),cardiac injury group (OVX+ISO+Vehi group),low dose estrogen treatment group (OVX+ISO+E2 a group,4μg·kg-1 ·d-1 ),high dose estrogen treatment group (OVX+ISO+E2 b group,40μg·kg-1 ·d-1 ). these status were separately measured:rats′general features,hemodynamics parameters monitored of carotid artery,morphological observation and cardiomyocyte contraction change of single-cardiomyocyte separate cultured,cardiomyocyte apoptosis protein ex-pression were detected by immunoblotting.Results ISO significantly reduced myocardial pump function,increased hypertrophy and apoptosis of cardiomyocytes,reduced contractility of single cardiomyocytes (P<0.05).High-dose estrogen (40μg·kg-1 ·d-1 ) replacement therapy significantly improved ISO induced cardio inj ury and cardio functions decreasing,also inhibited Bax expression and caspas-3 activation and decreased myocardial hypertrophy and cardiomyocytes apoptosis through increasing Bcl-2 expression (P<0.05),significantly.while low dose estrogen (4μg·kg-1 ·d-1 )treatment showed marginally protection effects on ISO in-duced cardio inj ury with no statisticly significance.Conclusion Appropriate dose estrogen replacement therapy can decrease cardio-myocyte apoptosis,improve cardiomyocytes contractility,so as to protect ISO-induced cardiomyocyte apoptosis.
