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作 者:姜正林[1] 吴新民 陈云[2] 金淑仪[1] 陈燕萍[3] 庄坚[1]
机构地区:[1]南通医学院航海医学研究所,江苏省南通226001 [2]南通医学院电镜室,江苏省南通226001 [3]白求恩医科大学基础医学院
出 处:《中华航海医学杂志》2000年第1期28-32,共5页
摘 要:目的 用离体海马脑片缺氧实验 ,结合电生理学和超微结构两方面的变化 ,研究人参皂甙的抗脑缺氧作用。方法 (1)观察大鼠离体海马脑片缺氧条件下顺向群峰电位 (orthodromic populationspikes,OPS)的变化及人参茎叶总甙对它的影响 ;(2 )同时观察缺氧后海马脑片 CA1区锥体细胞层超微结构变化及人参茎叶总甙对它的影响。结果 (1)在对照组海马脑片 ,缺氧时缺氧损伤电位出现率为 71.4% ,缺氧后 OPS恢复率为 14.2 % ,恢复程度为 (2 4.8± 31.9) % ;而使用人参皂甙的海马脑片在缺氧前即见OPS减小 ,缺氧时未出现缺氧损伤电位 (hypoxic injury potential,HIP) ,缺氧后 OPS恢复率和恢复程度分别为 10 0 %及 (10 9.5± 37.3) %。与对照组比较均有显著性差异。 (2 )电镜观察显示 ,缺氧组海马脑片的神经细胞呈变性至坏死等不同程度的损伤 ,而人参皂甙组脑片神经细胞与正常细胞相似 ,损伤较轻 ,突触结构清晰 ,兴奋性神经递质小泡无明显耗竭。结论 (1)人参皂甙有明显的抗缺氧脑损伤作用 ;(2 )人参皂甙抗脑缺氧作用机制可能是 :降低神经元兴奋性 ,减少能耗 ,并保护线粒体 ,以维持胞内 ATP水平 ;抑制兴奋性神经递质释放 ,减轻其兴奋毒性。Objective To investigate the protective effects of ginsenosides(GS) against anoxic injury electrophysiologically and morphologically in rat brain. Methods (1) Changes of orthodromic population spikes(OPS) in area CA1 of the hippocampal slice were observed during anoxia and after reoxygenation, and the influences on above changes in OPS were then investigated after administration of ginsenosides extracted from the leaf and stem of Panax ginseng; (2) Following above experiments, morphological changes of pyramidal neurons in CA1 region of hippocampal slice and the effects of GS on anoxic damage were observed. Results (1) In the slices treated with ginsenosides, hypoxic injury potential(HIP) did not occur, and the recovery amplitude and recovery rate of OPS were significantly higher than those of untreated slices; (2) With electromicroscopy, we found that the pyramidal neurons in CA1 region were injuried by anoxia ranging from degeneration to necrosis; however, in GS treated slices, anoxic damage of pyramidal neurons was reduced obviously, synaptic construction was maintained similar as normal, and consumption of excitatory neurotransmitter vesicles was reduced. Conclusions (1) Ginsenosides could protect brain cells from anoxic injury; (2) The mechanisms of this protective effect may be: GS could decrease the excitability of neurons and protect mitochondria from anoxic damage, thereby ATP level could be maintained; and GS may inhibit the release of excitatory neurotransmitter, thereby reducing its excitotoxicity.
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