The Cardioprotection And Mechanism Of Fisetin In A Isolated Rat Model Of Ischemia/Reperfusion Injury

Objective:To investigate the effect of fisetin on ischemia-reperfusion injury in isolated heart and its mechanism.Methods:The model of ischemia-reperfusion injury was prepared on Langendorff system.Qualified isolated heart models were randomly divided into four groups:Control,Model,Fisetin0.5(0.5 ?mol/L),Fisetin5(5 ?mol/L).The cardiac function parameters were measured by a biological function test system.The myocardial infarct size was measured by TTC staining.The content of CK-MB in perfusate and the levels of MDA,SOD,GSH,GSSG,IL-6 and TNF-a in myocardium were detected by enzyme-linked immunosorbent assay.Myocardial tissue morphology and cardiomyocyte apoptosis were measured by hematoxylin-eosin and TUNEL staining respectively.Results:Compared with the control group,the model group showed the following phenomena:the cardiac function parameters were significantly decreased,severe infarction and necrosis formed in the myocardium.The CK-MB of cardiomyocyte was released in large quantities.The activities of SOD and GSH were significantly decreased and the contents of MDA,GSSG,IL-6 and TNF-a were significantly increased in myocardium,and a large number of apoptotic cells appeared.Experimental findings suggest that ischemia and reperfusion can lead to severe injury.Compared with the model group,the pretreatment of fisetin could significantly reverse the changes of myocardial injury caused by ischemia-reperfusion.The myocardial protection of high-dose fisetin was more obvious.Conclusion:The fisetin can significantly reduce myocardium damage induced by ischemia-reperfusion,and it may be dose-dependent.The myocardial protection of fisetin may be related to its anti-oxidation,anti-inflammatory and anti-apoptotic effects.