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机构地区:[1]华中科技大学同济医学院
出 处:《郧阳医学院学报》2006年第2期81-83,共3页Journal of Yunyang Medical College
摘 要:目的:观察二氢石蒜碱(d ihydrolycorine,DL)对小鼠心肌缺血损伤的保护作用。方法:采用异丙肾上腺素(isoproterenol,Iso)致小鼠心肌缺血模型,检测DL对缺氧条件下小鼠存活时间及心肌缺血损伤后心肌组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、血清肌酸激酶(CK)和乳酸脱氢酶(LDH)活性的影响。结果:模型组缺氧条件下生存时间明显缩短,缺血损伤后心肌组织SOD活性显著下降,MDA含量明显升高,LDH和CK的活性明显升高,与正常组比较具有显著性差异(P<0.01);与模型组比较,随着药物剂量的增加,DL各剂量(15、30、60 mg.kg-1)组生存时间明显延长,SOD活性逐渐回升,MDA含量逐渐趋于恢复正常,LDH及CK活性均明显降低,以DL 30及60mg.kg-1组作用更显著(P<0.01或P<0.05)。结论:DL明显延长小鼠存活时间,抑制Iso致小鼠心肌缺血后血清CK和LDH活性升高,增加心肌组织总SOD活性,减少心肌组织MDA生成。DL对Iso诱导的小鼠心肌缺血损伤具有保护作用。Objective To investigate the protective effects of dihydrolycorine on myocardial ischemia injury induced by 30 mg · kg^-1 of isoproterenol sc in mice. Methods The myocardial ischemia injury model was developed by 30 mg kg^-1' of isoproterenol sc in mice. The survival time of mice, the activities of SOD and levels of MDA in myocardium, the activities of serum LDH and CK were all measured. Results The survival time of mice in the close normobaric hypoxia and the SO') activity in model group were decreased respectively after injured by isoproterenol, whereas the activity of LDH and CK and the content of MDA in model group were increased significantly (P 〈0.01 vs normal group). In mice injured by isoproterenol that were treated with 15, 30, 60 mg kg^ - 1 dihydrolycorine, LDH and CK release and MDA content were decreased, while the survival time and SOD activity were increased in dose -dependent manner (P 〈0.05 vs model group). Conclusion The results showed that dihydrolyeofine prolonged the survival time of mice in the close normobaric hypoxia, increased the activities of total SOD, and decreased the levels of MDA in myocardium. The activities of serum LDH and CK were also decreased. These results indicated that dihydrolycofine has protective effects on myocardial ischemia induced by isoproterenol in mice .
分 类 号:R541[医药卫生—心血管疾病]
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