Sinomenine exerts cardioprotective effects in a rat model of myocardial ischemia/reperfusion injury

Objective: To evaluate the cardioprotective effects of sinomenine using the ischemia/reperfusion (I/R) rat model. Methods: Wistar rats were randomly divided into 6 groups: group I with reperfusion, group II perfused with sinomenine, group III perfused with 5-hydroxydecanoate (5-HD), group IV perfused with 5-HD+sinomenine, group V perfused with L -nitro arginine methyl ester ( L -NAME), group VI perfused with L -NAME+sinomenine. Myocardial ischemia was induced by interrupting the aortic blood supply for 30 min, followed by reperfusion (55 min). Cardiac, hepatic, antioxidant, and inflammatory parameters were assessed. Additionally, endothelin, tissue factor, platelet-activating factor, plasminogen activator inhibitor, plasma fibrinogen, and thromboxane B2 were also analyzed. Results: Administration of 5-HD or L -NAME, used as the selective antagonist of mitoKATP and NO system, respectively, resulted in significantly increased levels of premature ventricular complexes, lactate dehydrogenase, ventricular fibrillation, ventricular tachycardia, and arrhythmia intensity ( P <0.05). In contrast, sinomenine significantly reduced the level of troponin I, lactate dehydrogenase, creatine kinase, and creatine kinase MB compared to the 5-HD group and the L -NAME group ( P <0.05). Additionally, sinomenine significantly reduced malondialdehyde level and enhanced the levels of superoxide dismutase, glutathione peroxidase, catalase, and glutathione/glutathione disulfide ratio ( P <0.05). It also significantly suppressed the levels of endothelin-1, platelet-activating factor, tissue factor, plasminogen activator inhibitor 1, thromboxane B2, and plasma fibrinogen ( P <0.05). Conclusions: These results suggest that sinomenine exhibits significant cardioprotection effects against I/R-induced cardiac injury in rats.