Myocardial infarction is a leading cause of mortality and morbidity worldwide. Although essential for successful recovery, myocardium reperfusion is associated with reperfusion injury. Icariin, a major flavonoid of Epimedium koreanum Nakai, has been proven to exert efficacy for improving cardiovascular function. We investigated the molecular effect and signal pathway of icariin on cardiac ischemia/reperfusion injury. In an in vivo model of infarct in rats, icariin (10 mg/kg) significantly attenuated myocardial infarct size induced by ischemia/reperfusion (I/R). From the TUNEL assay, icariin reduced the apoptotic cell induced by I/R and decreased blood indicators of creatine kinase, ischemia-modified albumin, and lactate dehydrogenase. All this effect was antagonized by the PI3K inhibitor LY294002. Meanwhile, icariin activated the PI3K/Akt/eNOS pathway. The PI3K inhibitor LY294002 suppressed icariin-mediated protective effect. These results suggest that icariin protects against myocardial ischemia reperfusion injury in rats by activating the PI3K/Akt/eNOS-dependent signal pathways and may be a useful drug for angiogenic therapy.
Animals Apoptosis