Protective effect of tanshinone IIA against myocardial hypertrophy in rats with pressure overload

AIM: To observe the changes of RhoA and Rock1 expressions in rat myocardial tissues with pressure overload and to explore the protective effects of tanshinone ⅡA(Tan IIA) against myocardial hypertrophy.METHODS: Thirty-two Sprague Dawley(SD) rats induced by abdominal aorta constriction preparation were randomly divided into four groups(each n=8): model group(P0.01),Tan ⅡA of low-dose group [L-Tan ⅡA group,10 mg/(kg·day)],Tan ⅡA of high-dose group [H-Tan IIA group,20 mg/(kg·day)],positive captopril group [captopril group,100 mg/(kg·day)] and age-matched SD sham-operated group(n=8) as control.The model of pressure overload-induced myocardial fibrosis was successfully established after 4 weeks of operation.After 4 weeks of Tan ⅡA treatment,heart mass indexes were estimated concurrently with evaluation of myocardial histology as well as myocardial hydroxyproline content by ELISA and immunohistochemistry staining and Western blot for myocardial RhoA and Rock1 content.RESULTS: Compared with those in sham group,heart mass indexes,myocardial hydroxyproline content and myocardial RhoA and Rock1 content were increased in the model group(P0.01).Compared with those in model group,heart mass indexes,myocardial hydroxyproline content and myocardial RhoA and Rock1 content were decreased in the L-Tan ⅡA group(P0.05),whereas these indexes were decreased significantly in the H-Tan ⅡA group(P0.01).CONCLUSIONS: Expressions of RhoA and Rock1 protein significantly increase in pressure overload rat myocardium,indicating that RhoA/Rock signaling pathways are involved in pressure overload in rat cardiac hypertrophy and occurrence and development of cardiac hypertrophy in rats with pressure overload.Tan ⅡA can alleviate cardiac hypertrophy possibly by downregulation of the expression of RhoA/Rock signaling pathways.