Objective To observe the changes of matrix metalloproteinases (MMPs), TIMP2, and inflammatory factors TNF-α and IL-1β in the myocardium of rats with acute myocardial infarction (AMI) treated with rosuvastatin.Methods Healthy SD rats were selected to establish an AMI model by ligation of the left anterior descending coronary artery.They were divided into four groups: a control group (isolation of anterior descending branch without ligation, n = 10); an acute myocardial infarction group (AMI modeling group); a rosuvastatin group (n =13, AMI treated with rosuvastatin at 10mg/ (kg·d) after modeling); and a losartan group (n = 11, AMI treated with losartan potassium at 5 mg/ (kg·d) after modeling). Immunohistochemical staining and RT-qPCR were used to determine the expression levels of MMP2, MMP9, and inhibitor TIMP2 in rat cardiac tissues after AMI modeling. Western blotting was used to determine the changes of MMP2,MMP9, TNF-α, and IL-1β in myocardium. Results The results of immunohistochemical and RT-qPCR analyses showed that, compared with those in the AMI group, the MMP2 and MMP9 protein/ mRNA expression levels in rat myocardium in the rosuvastatin and losartan groups were decreased ( P < 0. 05). Regarding the western blotting results, compared with that in the control group, the expressions of MMP9, MMP2, TNF-α, and IL-1β proteins in the AMI group were significantly increased( P <0. 05). Moreover, compared with those in the AMI group, the expression levels of MMP2, MMP9, TNF-α, and IL-1β in the myocardium of the rosuvastatin and losartan groups were decreased ( P <0. 05). Conclusions Myocardial fibrosis factors and inflammatory factors are increased after AMI modeling in rats. Rosuvastatin can improve the cardiac function to some extent by inhibiting myocardial fibrosis and reducing the expression of inflammatory factors.