Objective:To study the inhibition effects of simvastatin on cardiac hypertrophy induced by myocardial infarction

and to in-vestigate whether simvastatin prevents cardiac hypertrophy through attenuation of RhoA kinase.Methods:Male Wistar rats were divided intofourgroup(sn=8).Myocardial infarction model was established by ligation of left anterior descending coronary artery.Sham operati on group(SHAM group)and myocardidal infarction group(MI group)were gavaged with 0.9%NaCl 1ml/day

Simvastatin group(SIM group)was gavaged with simvastatin 40 mg/(kg.d).Fasudil group(F group)was injected with fasudil 7.5mg(/kg.bid)through peritoneum.At the time point of 28 ds

the ratio of LV weight to body weight(LVW/BW)and the cross-sectional area of cardiomyocytes were measured.The mRNA expression level of ROCK was detected by RT-PCR.The expression level of Phosphorylated-ERM was detected by immunohisto-chemistry and Western blot.Results:28ds after MI

the LVW/BW

the cross-sectional area of cardiomyocytes

the mRNA expression level of ROCK and the expression level of Phosphorylated-ERM significantly increased in the MI group compared with those in the SHAM group.And the indexes mentioned above significantly decreased both in the SIM group and F group compared with those in the MI group.Conclusion:Simvastatin prevents post-infarcted cardiomyocyte hypertrophy partly through inhibition of ROCK.