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作 者:张广钦[1] 陈世忠[2] 郝雪梅[1] 程和平[1] 吴才宏[1]
机构地区:[1]北京大学生物膜与膜生物工程国家重点实验室,北京100871 [2]北京大学药学院中药研究室,北京100083
出 处:《中国药理学通报》2003年第9期1020-1023,共4页Chinese Pharmacological Bulletin
基 金:国家中医药管理局重大科技开发项目资助课题 No国中发 [2 0 0 1]10号
摘 要:目的 研究厚朴酚对脑缺血的保护作用。方法 采用小鼠常压耐缺氧实验 ,测定小鼠氧耗量及存活时间 ;小鼠双侧颈总动脉结扎引起急性不完全脑缺血模型 ,测定小鼠死亡时间 ;大鼠大脑中动脉阻塞法 (MCAO)造成局灶性脑缺血模型 ,评价动物行为功能 ,测定脑梗死范围及脑组织中SOD、MDA及LDH的含量 ,并进行病理学组织检查。结果 厚朴酚能剂量依赖性地延长小鼠缺氧缺血的存活时间 ;改善大鼠脑缺血造成的行为缺陷 ,提高脑组织中SOD和LDH活性 ,减少MDA含量 ,缩小梗死范围 ,降低脑含水量。病理学组织检查显示 ,厚朴酚能改善脑缺血造成的大鼠神经细胞的损伤 ,减少组织坏死。结论 厚朴酚对脑缺血有保护作用 。AIM To study the protective effect of magnolol (Mag) on cerebral ischemia. METHODS Anoxia was produced by close normobaric hypoxia; acute incomplete cerebral ischemia was induced by ligaturing bilateral carotid arterise; the local cerebral ischemia was made by middle cerebral artery occlusion. Superoxide dismutase (SOD), malondialdehyde (MDA) and lactate dehydrogenase (LDH) were meassured. The extent of neurologic deficit and the pathological change of cerebral tissues were observed. RESULTS Mag, in a dose dependent manner, prolonged survival time of mice in the states of anoxia and ligaturing bilateral carotid arterise. In the MCAO model, Mag markedly ameliorated rat neurologic deficit. It could also increase the activities of SOD and LDH, reduce MDA and water contents, dwindle infarct zone in cerebral tissues. The pathological examination showed that Mag could significantly protect brain from ischemia reperfusion injury, reduce the necrosis of neuron and the cerebral infarction silte. CONCLUSIONS Mag has a protective effect against ischemia brain damage by its antioxidant activity.
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