Effects of simvastatin on ERK1/2 signaling pathway and ventricular myocardium collagen change after myocardial infarction in rats

Objective:To investigate the effect of simvastatin on heart function,Ⅰ and Ⅲ type of ventricular myocardium collagen,extracellular regulated protein(ERK1/2),and phosphorylated ERK1/2 expression in rats model of acut myocardial infarction(AMI).Methods:Acute myocardial infarction(AMI) was established by ligation of the anterior descending coronary artery in rats.Twenty-four hours after the procedure,the 30 surviving rats were grouped randomly as AMI(A) group(n=10) and simvastatin(S) group(n=15).Other six rats which received the sham-operation(same procedure without ligation) were selected as control(C) group.The rats were killed 8 weeks later after examining hemodynamic parameters,body weight(BW),left and right ventrieular weight(LVw,RVw),the expression of ERK1/2,and P-ERK1/2 protein in myocardium were evaluated by Western blot.Results:There were no significant differences between the AMI group and simvastatin group in infarction size(P0.05),left ventricular section diameter,area and left ventricular volume.In comparison with the AMI group,LVW、LVW/BW and left ventricular en-diastolic pressure(LVEDP) were significantly increased in the AMI group(P0.01),the maximal rate of rise and fall(±dp/dt) and their adjustment by LVSP(±dp/dt/LVSP) were significantly increased(P0.05) in simvastatin group.Compared with the AMI group,Ⅰ and Ⅲ type of myocardium collagen in the infracted zone and phosphorylation of ERK1/2 were all significantly decreased in simvastatin group,Ⅰ and Ⅲ type of myocardium collagen in the infracted zone content were both positively correlated with phosphorylation of ERK1/2(r=0.916 and 0.983,respectively,P0.01).Conclusion:Simvastatin showes favorable effects on left ventricular remodeling after AMI in rats and demonstrated improved cardiac function.These effects could be relevant to the attenuation of ERK1/2 phosphorylation.