AimTo investigate the effects of 17β-estradiol on myocardial hypertrophy induced by testosterone, and to explore the role of ERK1/2 protein in the signal transduction pathway of sexual hormone in development of myocardial hypertrophy.MethodsMyocardial cells were isolated from ventricles of 1～3-day-old neonate rats purified by a culture method based on Simpson.Neonate rat cardiomyocyte hypertrophic responses were assayed by measuring protein content, protein synthesis rate.Expression of protein ERK1/2 was detected by Western blot.Results17β-estradiol (E₂) was able to inhibit the increase of cell protein and ³H-Leu incorporation induced by T in a range from 10^－10～10^－6 mol/L, with an optimal concentration of 10^－8 mol/L.The effect of E₂ was partly intercepted by Tamoxifen.The inhibitory effect of E₂ on the increase of ³H-Leu incorporation in cardiomyocytes induced by testosterone was not enhanced by PD98059.The increased expression of ERK1/2 induced by testosterone was reversed by E₂ at concentration of 10^－8 mol/L.The increased expression of ERK1/2 induced by testosterone which was inhibited by E₂ was reversed by pretreating with Tamoxifen (10^－6 mol/L) for 2 h.ConclusionE₂ could reverse the myocardial hypertrophy induced by testosterone by inhibiting the expression of ERK1/2, which was mediated by estrogen receptor.