Simvastatin prevents rat cardiac hypertrophy induced by myocardial infarction via RhoA kinase
Jiwei Huang
Abstract
Jiwei Huang
Abstract
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.
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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.
Key concepts: Simvastatin, Fasudil, RHOA, Medicine, Internal medicine, Myocardial infarction, Cardiology, Muscle hypertrophy