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机构地区:[1]中国科学院上海生命科学研究院上海药物研究所新药研究国家重点实验室,上海中国200031
出 处:《Acta Pharmacologica Sinica》2002年第12期1193-1198,共6页中国药理学报(英文版)
基 金:Project supported by the National Natural Science Foundation of China № 3001161954,301230050.
摘 要:AIM: To test the ability of huperzine B (HupB) to alleviate injury from oxygen-glucose deprivation (OGD) in the rat pheochromocytoma line PC12 cells. METHODS: After OGD for 3 h and reoxygenation for 24 h, neuronal mor-phology was observed by phase-contrast microscopy; cell survival was quantified by the reduction of MTT; malondialdehyde (MDA) was determined by the thiobarbituric acid; superoxide dismutase (SOD) was assayed by a modification of the xanthine/xanthine oxidase; and lactate (LA) was measured according to Marbach and Weil. RESULTS: OGD for 3 h and reoxygenation for 24 h triggered death in nearly 70 % of cells, along with major changes in morphology and biochemistry including elevated level of MDA, SOD activity, and LA content. Cells pretreated with HupB 1-100 μmolfL for 2 h showed significantly improved survival and reduced biochemical and morphologic signs of toxicity. CONCLUSION: HupB protected PC12 cells against OGD-induced injury, most likely by alleviating disturbances of oxidative and energy metabolism.目的:研究石杉碱乙(HupB)对氧糖缺乏培养所致PC12细胞损伤的保护作用.方法:氧糖缺乏培养3小时再氧化24小时后,用倒置相差显微镜观察细胞形态;噻办公(MTT)法检测细胞存活率;硫代巴比妥酸法测定细胞丙二醛(MDA)含量;黄嘌呤氧化酶法测定细胞超氧化物歧化酶(SOD)活力;Marbach及 Weil方法测定细胞乳酸(LA)含量.结果:氧糖缺乏培养3小时再氧化24小时诱发约70%的细胞死亡,细胞形态发生明显改变,MDA、SOD及LA等生化指标明显升高.HupB(1-100 μmol/L)预孵育2小时,能明显提高细胞存活率,改善细胞形态,降低各项生化指标.结论:HupB对氧糖缺乏所致细胞损伤保护作用可能与调节氧化能量代谢失衡有关.
关 键 词:huperzine B cholinesterase inhibitors MALONDIALDEHYDE superoxide dismutase LACTATES PHEOCHROMOCYTOMA
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