Study on the mechanism of rosuvastatin in improving the cardiac function of the rabbits with myocardial infarction

Objective To investigate the effects of rosuvastatin on ventricular remodeling after myocardial infarction and the potential mechanism.Methods Forty-five male New Zealand albino rabbits were randomly divided into three groups: sham operation(S) group(n = 15),myocardial infarction(MI) group(n = 15) and rosuvastatin intervention(R) group(n = 15).AMI animal models were established with the ligation of left anterior descending coronary artery in MI group and R group.Rabbits in R group were administered with rosuvastatin at a dose of 10mg /(kg·d) via direct gastric gavage 24 hours after the ligation;while rabbits in the other two groups were administered with same volume of distilled water via gastric gavage at the same time.After two weeks,all the rabbits were killed,and the hearts were taken out to detect apoptosis by TUNEL.The expression of Caspase-3 at the myocardial infarction edge area was measured by flow cytometry,and the expressions of p38,p-p38 in protein level were measured by western blot.Results Compared with MI group,the left ventricular end diastolic diameter(LVEDD) and left ventricular end systolic diameter(LVESD) in R group were smaller,but the left ventricular ejection fraction(LVEF) was higher.There was no significant difference between R group and MI group in the expression of p38.However,there were significant differences in Caspase-3 and p-p38 expression in the tissue of the myocardial infarction edge area between R group and MI group.Conclusions Rosuvastatin may suppress ventricular remodeling and improve cardiac function by preventing cardiomyocyte apoptosis through restraining phosphorylation of p38 and preventing Caspase-3 activation.