Simvastatin Therapy On CT-1 Gp130 After AMI And Its Relativity With Left Ventricular Remolding

Objective to study the inhibition effect of simvastain on left ventricular remolding(LVRM) induced by acute myocardial infarction,and to investigate whether simvastatin prevent left ventricular remolding through attenuation of carditrophin-1—gp130.Methods Male SD rats were divided into four groups (n=8).:AMI group,AMI +Simvastatin group,Sham-operated group and normal group. Myocardial infarction model of the first two groups was established by ligation of left anterior descending coronary artery. AMI +Simvastatin group was gavaged with simvastatin 40mg/(kg·d).Rats except Simvastatin treatment group were gavaged with part. aeq.0.9% NaCl. After 4 weeks, the ratio of LV weight to body weight(LVWI), the cross-sectional area of cardiomyocytes(CSA) and the collagen volume fraction(CVF) were examined.The CT-1 and gp130 mRNA expression in non-infarction zone in left ventricular (LVNIZ) was determined by RT-PCR. The CT-1 and gp130 protein production in LVNIZ was determined by Western blot.Results Compared with sham—operated rats and normal rats,left ventricular weight index(LVWI), cardiomyocyte cross-sectional area(CSA) and CVF in LVNIZ were increased (P <0.05) in AMI group,the expression of CT-1,gp130 mRNA and production of CT-1,gp130 protein in LVNIZ increased obviously after AMI 4 weeks(P <0.05).CT-1,gp130 mRNA expression and protein production were all decreased in AMI +Simvastatin group with lightened LVRM comparing with AMI group(P <0.05).Conclusion:1 There is significant correlation between overexpression of CT-1,gp130 mRNA and protein and LVRM after AMI.2 The mechanisms of simvastatin in preventing LVRM may be partly through depressing CT-1,gp130 mRNA expression and protein production.