Objective: To explore the protective effect of rosuvastatin combined with ischemic post-treatment in protecting myocardium in diabetic rats and analyze its protective mechanism. Methods: The rats animal model of type 2 diabetes mellitus was constructed by high fat and high sugar diet, and they were randomly divided into sham operation group (sham group), ischemia/reperfusion group (I/R group), ischemic post-treatment group (IpostC group) and rosuvastatin combined with ischemic post-treatment group (RPO+IpostC group), with 10 rats in each group. The expressions of hypoxia-inducible factor-1 α (HIF-1α) and inducible nitric oxide synthase (iNOS) protein, the levels of plasma inflammatory factors and serum nitric oxide (NO) in each group were analyzed, and the changes of myocardial infarction size and HE staining structure in myocardial tissue were observed in each group. Results: Compared with I/R group and IPostC group, the expression of HIF-1α and iNOS protein in RPO+ IPostC group were significantly up-regulated (P<0.05). Compared with IpostC group, the levels of serum NO and plasma IL-1β, IL-6 and TNF- α in RPO+ IpostC group were significantly decreased, while plasma IL-10 was increased (P<0.05). Microscopic observation showed that the myocardial cells in the sham group had normal HE staining structure, while the myocardial cells in the RPO+IpostC group had relatively little damage after HE staining. Compared with I/R group, ischemic area (AAR/LV), infarct area (IRR/AAR) of rats in IpostC group and RPO+IpostC group were significantly decreased, and AAR/LV and IRR/AAR in RPO+IpostC group were the least (P<0.05). Conclusion: Rosuvastatin combined with ischemic post-treatment can regulate the HIF-1α-iNOS signaling pathway in diabetic rats, raise the expression of HIF-1α and iNOS protein, alleviating inflammatory response, reducing myocardial ischemia-reperfusion injury, and protecting myocardium. |