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目的:观察白藜芦醇预处理对体外大鼠缺血再灌注心肌损伤的保护作用及其作用机制。方法:利用Langendorff灌注系统,建立体外大鼠心肌常温全心心肌缺血30min再灌注120min损伤模型。将56只雄性SD大鼠随机分为4组(每组14只):缺血再灌注损伤(IRI)组、白藜芦醇组、Nω硝基L精氨酸甲酯(LNAME)组、氨基胍(AG)组。检测各组的心功能、心肌一氧化氮合酶(NOS)同工酶(NOSi)活性、一氧化氮(NO)的含量、丙二醛的含量、心肌梗死面积以及心肌细胞凋亡指数。结果:与IRI组相比,白藜芦醇组左室发展压(LVDP)、左室压力上升和下降最大变化速率(±dp/dtmax)明显改善(P<0.05或0.01);心肌梗死面积、心肌细胞凋亡指数、心肌丙二醛含量显著降低(P<0.01);心肌NOSi活性和NO含量显著升高(P<0.01)。LNAME组和AG组LVDP和±dp/dtmax显著低于白藜芦醇组(P<0.05或P<0.01);心肌梗死面积、心肌细胞凋亡指数、心肌丙二醛含量显著升高(P<0.01);心肌NOSi活性和NO含量显著降低(P<0.01)。结论:白藜芦醇对体外大鼠IRI具有保护作用,其机制可通过提高心肌NOSi活性,促进NO产生而介导的。
OBJECTIVE: To observe the protective effect of resveratrol pretreatment on myocardial injury induced by ischemia-reperfusion in rats and its mechanism. METHODS: The Langendorff perfusion system was used to establish a rat model of myocardial ischemia at room temperature for 30 min and reperfusion for 120 min. 56 male SD rats were randomly divided into 4 groups (14 in each group): ischemia-reperfusion injury (IRI) group, resveratrol group, Nω-nitroL-arginine methyl ester (LNAME) group, amino group胍 (AG) group. Cardiac function, myocardial nitric oxide synthase (NOS) isoenzyme (NOSi) activity, nitric oxide (NO) content, malondialdehyde content, myocardial infarct size, and cardiomyocyte apoptosis index were measured in each group. RESULTS: Compared with the IRI group, the left ventricular development pressure (LVDP), the maximum rate of change in left ventricular pressure rise and fall (±dp/dtmax) were significantly improved in the resveratrol group (P<0.05 or 0.01); myocardial infarct size, Cardiomyocyte apoptotic index and myocardial MDA content were significantly decreased (P<0.01); myocardial NOSi activity and NO content were significantly increased (P<0.01). LVDP and ±dp/dtmax were significantly lower in the LNAME and AG groups than in the resveratrol group (P<0.05 or P<0.01); myocardial infarct size, myocardial cell apoptosis index, and myocardial MDA content were significantly higher (P< 0.01); myocardial NOSi activity and NO content were significantly reduced (P <0.01). Conclusion: Resveratrol has a protective effect on rat IRI in vitro, and its mechanism can be mediated by increasing myocardial NOSi activity and promoting NO production.