Osthole Attenuated Myocardial Ischemia/Reperfusion Injury Via A Mitochondrial Apoptosis

The mitochondrion plays an important role in myocardial ischemia/reperfusion (MI/R) injury. Osthole, a bioactive coumarin derivative extracted from medicinal plants, has been shown to have protective properties in ischemic disease. The aims of the present study were to explore whether Osthole could attenuate myocardial I/R injury and to investigate the potential mechanisms involved. The I/R model was established in vivo in SD rats. To evaluate the protective effects of Osthole on I/R injury, we measured the hemodynamics, myocardial pathological change and the expression of CK, LDH, BCL-2, Bax, BCL-XL, Caspase3, Cleaved-Caspase3, Caspase9 and Cleaved-Caspase9. We also explored the potential mechanisms by investigating mitochondrial function as demonstrated by the ROS, ATP content, translocation of cytochrome c and AIF. Pretreatment with Osthole can significantly decrease the serum CK and LDH level, the pathological and hemodynamic changes, the ROS level, the expression level of cleaved-Caspase3, cleaved-Caspase9, Bax, cytoplasmic cytochrome C and AIF in MI/R injury with the up-regulation of Bcl-2, BCL-XL, Caspase3 and Caspase9. Our results implied that Osthole may protect rats against MI/R injury by preventing ROS-induced mitochondrial apoptosis.