Effect of TanshinoneIIA on MAPK signaling pathway in cardiomyocytes hypertrophy induced by AngII

Objective To observe effects of Sodium tanshinoneⅡA sulfonate(STS)on angiotensionⅡ(AngⅡ)-induced cardiomyocyte hypertrophy and the expression of phosphorylated mitogen-activated protein kinase(p-MAPK).Methods In the primary culture of neonatal rat cardiomyocytes,as indexes of cardiomyocyte hypertrophy,the total protein was determined by coomassie brilliant blue and protein synthesis rate was measured by[~3H]-Leucine incorporation.The expression of p-MAPK was assessed u- sing Western blot.Results①The total protein and protein synthesis rate stimulated by AngⅡ(1μmol/L)in the cardiomyocytes in- creased significantly in contrast to control;STS can effectively decrease the increased total protein level induced by AngⅡand marked- ly inhibited syntheses of protein.②Pretreatment of cardiomyocyte with AngⅡ(1μmol/L)for 5 rain,the p-MAPK(p44MAPK/ p42MAPK)protein expression began to increase,the peak effect was at 10 rain.While pretreatment with STS(2,10,50μmol/L), AngⅡ-induced increase in p-MAPK were inhibited evidently.③Pretreatment cardiomyocyte with STS in different dose for 30min, we find STS can inhibit the expression of p-MAPK stimulated by AngⅡin a dose-dependent manner.Conclusion The results sug- gest that activation of MAPK may play an important role in cardiomyocytes hypertrophy induced by AngⅡ,and the anti-hypertrophic effect of STS on cardiomyocyte hypertrophy induced by AngⅡmay be associated to it's effect of inhibition to MAPK signaling pathway.