动物造模,离体心脏缺血再灌注损伤 z-bio 2022-02-28 534

　　Objective: To study the protective effect and mechanism of myricetin on ischemia-reperfusion injury in isolated rat hearts.

　　Methods: 60 SD rats were randomly divided into 6 groups: normal control group, model group, positive administration group (verapamil 100 μg/L) and myricetin low, middle and high dose group (2.5, 5, 10 mg/L). ), 10 in each group. The Langendorff isolated heart perfusion technique was used to stop perfusion for 30 minutes and reperfusion for 45 minutes to create a model of myocardial ischemia-reperfusion injury. The effects of myricetin on cardiac hemodynamic indexes were recorded, the levels of myocardial trienzymes LDH, CK and AST in coronary effluent, the activities of antioxidant enzymes SOD and CAT in myocardial tissue and the content of lipid peroxide MDA were measured. . Histopathological changes of myocardial tissue were observed by HE staining. The expression of apoptosis-related proteins was detected by Western blot.

　　Results: The cardiac hemodynamic indexes of the rats in the myricetin low, medium and high dose groups were significantly improved, the release of LDH, CK and AST in coronary effluent decreased, the activities of SOD and CAT in myocardial tissue increased, and the production of MDA decreased. reduce myocardial damage caused by ischemia-reperfusion. Western blot results showed that myricetin could up-regulate the expression of Bcl-2, down-regulate the expression of Bax, Caspase-3 and Caspase-9, and inhibit the phosphorylation of ERK.

　　Conclusion: Myricetin has a protective effect on myocardial ischemia-reperfusion injury, can improve myocardial contractile function, enhance antioxidant capacity, inhibit cell apoptosis, etc. The mechanism may be caused by inhibiting ERK signal transduction pathway to relieve ischemia-reperfusion. Cardiomyocyte apoptosis.