Abstract: Objective To explore the role of ERK1/2 protein in the signal transduction passway of testosterone（T） in development of myocardial hypertrophy. Methods Myocardial cells were isolated from ventricles of 1~3-day-old neonate rats purifed by a culture method based on Simpson. Neonate rat cardiomyocyte hypertrophic responses were assayed by measuring protein content, protein synthesis rate and cell surface area. Expression of protein ERK1/2 were detected by western blotting. Results Cell protein content, 3H-leucine (3H-leu) incorporation and cell surface area increased by treating of cardiomyocytes with T (10-10～10-6mol/L) for 24h. The maxium effect was observed at the concentration of 10-8mol/L. The increase of cell protein content induced by T could be inhibited by pretreating with Flutamide (10-5mol/L) for 2h, while there had no effect on cardiomyocytes pretreating with Flutamide alone. The increase of 3H-leu incorporation induced by T was largely blocked by PD98059（50μmol/L）. Expression of ERK1/2 was upregulated significantly by treating with testosterone for 24h at the level of 10-8mol/L. The increased expression of ERK1/2 induced by T was reversed by pretreating with Flutamide(10-5mol/L) for 2h. Conclusion T with physio-concentration could induce cardiomyocyte hypertrophy and this effect was possibly mediated through the activation of ERK1/2 signalling. During this procession, T upregulated the protein expression of ERK1/2 mediated by androgen receptor.

Key words: testosterone, cardiomyocyte hypertrophy, ERK1/2, signal transduction