关键词: 促红细胞生成素，心肌细胞肥大，TGF-β1，TAK1，p38MAPK

Abstract: Objective To observe the effects of erythropoietin ( EPO) on angiotensinⅡ ( AngⅡ ) induced neonatal rat cardiomyocyte hypertrophy and its signal protein expression. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and were used to establish the model of hypertrophy by AngII in vitro.The cells was treated with EPO or/and P38MAPK inhibitor SB203580. The cell surface area, [3H]-leucine incorporation ,mRNA expression of atrial natriuretic factor(ANF) and β-myosin heavy chain(β-MHC) of cardiomyocytes were employed to detect cardiomyocyte hypertrophy. The mRNA levels of TGF-β1 and P38MAPK was analyzed by real-time quantitative PCR. The protein expression of TGF-β1、TAK1、P38MAPK and phosphorylation of TAK1 and P38MAPK were analyzed by Western blot. Results EPO attenuated hypertrophy of cardiomyocytes. EPO significantly suppressed TGF-β1、TAK1、P38MAPK、phosphrylation of TAK1 and P38MAPK expression. SB203580 represses cardiac hypertrophy. Conclusions EPO attenuates cardiomyocytes hypertrophy induced by Ang II,and it might be associated with TGF β1-TAK1-P38MAPK signaling pathway.

Key words: erythropoietin，cardiocyte hypertrophy，TGF-β1，TAK1，p38MAPK