Objective:To observe the effects of sodium tanshinoneⅡA sulfonate(STS) on angiotensinⅡ(AngⅡ)-induced hypertrophy of myocardial cells through the expression of phosphorylated extracellular signal-regulated kinase(p-ERK1/2).Methods:In the primary culture of neonatal rat myocardial cells,the total protein content in myocardial cells was determined by coomassie brilliant blue and the protein synthesis rate was measured by[3H]-Leucine incorporation as indexes for hypertrophy of myocardial cells.The expression of p-ERK1/2 was determined using Western blot and immunofluorescence labeling.Results:(1)The total protein and protein synthesis rate increased significantly in contrast to the control group after the myocardial cells were stimulated by AngⅡ(1μmol/L)for 24 h;STS markedly inhibited the increment of the total protein level induced by AngⅡand the syntheses of protein.(2)After pretreatment of myocardial cells with AngⅡ(1μmol/L)for 5 min,the p-ERK1/2 protein expression was increased,with the most obvious effect shown at about 10 min;pretreatment of myocardial cells with STS at different doses(2,10, 50μmol/L)for 30 min resulted in obvious inhibition of the expression of p-ERK1/2 stimulated by AngⅡin a dose-dependent manner.(3)After the myocardial cells were stimulated by AngⅡ(1μmol/L), the immunofluorescence of ERK1/2 rapidly appeared in the nucleus.The activation and translocation process of ERK1/2 induced by AngⅡwas blocked distinctly by STS.Conclusion:STS inhibited the myocardial cell hypertrophy induced by AngⅡ,and the mechanism may be associated with the inhibition of p-ERK1/2 expression. Objective: To observe the effects of sodium tanshinoneIIA sulfonate(STS) on angiotensinII(AngII)-induced hypertrophy of myocardial cells through the expression of phosphorylated extracellular signal-regulated kinase(p-ERK1/2).Methods:In the primary culture of neonatal Rat myocardial cells,the total protein content in myocardial cells was determined by coomassie brilliant blue and the protein synthesis rate was measured by[3H]-Leucine incorporation as indexes for hypertrophy of myocardial cells.The expression of p-ERK1/2 was determined using Western blot and immunofluorescence labeling.Results:(1)The total protein and protein synthesis rate increased significantly in contrast to the control group after the virus cells were stimulated by AngII(1μmol/L) for 24 h;STS markedly inhibited the increment of the Total protein level induced by AngIIand the syntheses of protein.(2)After pretreatment of myocardial cells with AngII(1μmol/L) for 5 min,the p-ERK1/2 protein expression was inc Reased, with the most obvious effect shown at about 10 min;pretreatment of myocardial cells with STS at different doses(2,10, 50μmol/L) for 30 min resulted in obvious inhibition of the expression of p-ERK1/2 stimulated by AngIIin a dose-dependent manner.(3)After the virus cells were stimulated by AngII(1μmol/L), the immunofluorescence of ERK1/2 rapidly appeared in the nucleus.The activation and translocation process of ERK1/2 induced by AngIIwas blocked distinctly by STS.Conclusion: STS inhibited the myocardial cell hypertrophy induced by AngII, and the mechanism may be associated with the inhibition of p-ERK1/2 expression.