动物实验,杨梅苷,心脏缺血 z-bo 2020-08-25 520

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

　　Methods: 60 SD rats were randomly divided into 6 groups: normal control group, model group, positive dose group (verapamil 100μg/L), myricetin low, medium and high dose groups (2.5, 5, 10) Mg/L). ), 10 per group. Using Langendorff isolated heart perfusion technique, stop perfusion for 30 minutes and then reperfusion for 45 minutes to create a model of myocardial ischemia-reperfusion injury. Record the effect of myricetin on cardiac hemodynamic indicators to determine the levels of three myocardial enzymes LDH, CK and AST in coronary effluent, the activity of antioxidant enzymes SOD and CAT in myocardial tissue, and the content of lipid peroxidation MDA Do it. HE staining to observe the pathological changes of myocardial tissue. Western blot was used to detect the expression of apoptosis-related proteins.

　　Results: Rat cardiac hemodynamics at low, medium and high doses of myricetin were significantly improved, the release of LDH, CK and AST in coronary effluent decreased, SOD and CAT activity in myocardial tissue increased, and MDA production decreased. Reduce myocardial damage caused by different degrees of ischemia and reperfusion. Western blot results showed that myricetin can up-regulate the expression of Bcl-2, down-regulate the expression of Bax, caspase-3 and caspase-9, and inhibit ERX phosphorylation.

　　Conclusion: Myricetin has a protective effect on myocardial ischemia-reperfusion injury, can improve myocardial contractility, enhance antioxidant capacity, and inhibit cell apoptosis. The mechanism is to reduce ischemia and reperfusion by inhibiting the ERK signaling pathway caused by cardiomyocyte apoptosis.