动物造模,急性心肌梗死 z-bio 2022-09-30 562

　　Objective: To observe the changes of matrix metalloproteinase MMPs, TIMP2 and inflammatory factors TNF-α and IL-1β in myocardial tissue of rats with acute myocardial infarction (AMI) treated with rosuvastatin.

　　METHODS: Healthy SD rats were selected to establish an AMI model by ligating the left anterior descending coronary artery. They were divided into 4 groups, control group (only threading without ligation of coronary artery, n=10); acute myocardial infarction group (n=14); Rosuvastatin group (n=13): treated with rosuvastatin (10 mg/(kg·d)) after AMI modeling; Losartan group (n=11): treated with losartan potassium after AMI modeling treatment (5 mg/(kg·d)). Immunohistochemistry and RT-qPCR were used to detect the expression levels of matrix metalloproteinase mmp2, mmp9 and inhibitor TIMP2 in myocardial tissue of rats after AMI modeling, and Western blot was used to detect the expression levels of myocardial tissue in myocardial tissue. Protein changes of mmp2, mmp9 and inflammatory factors TNF-α and IL-1β.

　　Results: The results of immunohistochemistry and RT-qPCR showed that compared with the AMI group, the myocardial mmp2 and mmp9 protein and mRNA expression levels of the rosuvastatin group and the losartan group were decreased (P<0.05); Western blot detection Results: Compared with the control group, the expressions of mmp9, mmp2, TNF-α, IL-1β protein in the AMI group were significantly increased (P<0.05); The protein expression levels of mmp2, mmp9, TNF-α and IL-1β in the myocardium of the rats in the sartan group were all decreased (P<0.05).

　　Conclusion: The myocardial fibrosis factors mmp2, mmp9 and inflammatory factors TNF-α and IL-1β are increased after AMI modeling in rats, and rosuvastatin can inhibit myocardial fibrosis and reduce the expression of inflammatory factors in a certain degree. improve cardiac function to a certain extent.