Rosuvastatin inhibits inflammatory response and resists fibrosis after myocardial infarction.

OBJECTIVE: To study the effect of rosuvastatin on myocardial infarction in rats and its mechanism of action. MATERIALS AND METHODS: 24 Sprague-Dawley (SD) rats were randomly divided into 3 groups: intensive statin group (n=8), myocardial infarction control group (n=8) and sham-operation group (n=8). The left anterior descending coronary artery was ligated to establish myocardial infarction models. Rats in intensive statin group were treated with gavage via rosuvastatin (1 mg × kg) and 1.5 mL distilled water suspension at 3 d before operation, while rats in the other two groups received gavage via the same amount of distilled water till 4 weeks after operation. Venous blood was collected using capillary glass tubes at 3 d before operation (before medication) and the last day in the 4th week after operation. Interleukin-6 (IL-6) was detected via chemiluminescence assay, and tumor necrosis factor-α (TNF-α) was detected via immunofluorescence assay. Hematoxylin and eosin (HE) staining and Masson staining were performed for myocardium to detect the inflammation and fibrosis. Finally, the expressions of inflammatory protein p65, peroxisome proliferator-activated receptor (PPAR) and fibrin were detected via Western blotting, and the Snail expression was detected by immunohistochemical assay. RESULTS: The survival rate and cardiac function of rats in intensive statin group were superior to those in control group. HE staining and detection of blood IL-6 and TNF-α, and p65 and PPAR protein expressions revealed that the inflammatory levels in the body and myocardium of rats in intensive statin group were decreased compared with those in control group. Masson staining and detection of fibrin level showed that the myocardial fibrosis level of rats in intensive statin group was reduced compared with that in control group. CONCLUSIONS: Rosuvastatin can reduce the level of myocardial fibrosis through alleviating the inflammatory response in rats with myocardial infarction.