Mechanisms of total flavones of Epimedium on oxidative stress induced by myocardial ischemia/reperfusion injury in rats

To investigate the effects and mechanisms of total flavones of Epimedium (TFE) on oxidative stress induced by myocardial ischemia/reperfusion injury in rats, forty male SD rats were randomly divided into sham operated group, model group, diltiazem group and flavonoids of Epimedium low and high doses groups with 8 rats in each. Myocardial ischemia/reperfusion injury model was induced by ligaturing the left anterior descending artery for 30 min followed reperfusion for 4 h after TFE was taken by intragastric administration for 4 days. The degree of myocardial infarct was observed by N-BT staining. The concentrations of MDA and activities of SOD and T-AOC in cardiac tissue were measured by colorimetry. Serum TnI concentrations were checked by ELISA. HE stain was used to observe myocardium structure under light microscope. Expressions of SIRT1 and Nrf2 in cardiac tissue were evaluated by immunohistochemistry method and Western blot, respectively. Compared with the model group, the degree of myocardial infarct, MDA concentration in cardiac tissue and the levels of TnI in serum significantly decreased in the diltiazem group and flavonoids of Epimedium low and high doses groups (P<0.05 or P<0.01); flavonoids of Epimedium low and high doses groups and the diltiazem group also showed improvements in myocardium structure under ischemia/reperfusion injury. TFE significantly increased the activity of SOD and T-AOC and the expression of SIRT1 and Nrf2 in cardiac tissue when compared with the model group (P<0.05 or P<0.01). Therefore, TFE can increase anti-peroxidant capacity of myocardium tissue by using intrinsically anti-oxidant signaling pathway of SIRT1 and Nrf2, which can inhibit irreversible damage of cardiomyocytes in myocardial ischemia/reperfusion injury and protect normal function of cardiac tissue.