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机构地区:[1]锦州医学院药理学教研室,辽宁锦州121001 [2]潍坊医学院卫生法学教研室,山东潍坊261042
出 处:《锦州医学院学报》2004年第4期1-4,共4页Journal of Jinzhou Medical College
摘 要:目的 研究阿魏酸钠 (SF)对 β淀粉样蛋白2 5-3 5(Aβ2 5-3 5)诱导的原代培养神经细胞损伤的保护作用。方法 以原代培养孕 17~ 18d的SD大鼠胎鼠的大脑皮层神经细胞为观察对象。倒置显微镜下观察给药前后神经细胞的形态学变化 ,用MTT比色实验检测神经细胞活性 ,依据LDH漏出率检测神经细胞膜的损伤程度 ,以MDA生成量推测生物膜不饱和脂肪酸过氧化程度。结果 与正常对照组相比 ,Aβ2 5-3 5(2 0 μmol/L)处理 2 4h ,可使神经细胞活性显著下降 (P <0 0 1) ,SF (10 μmol/L ,5 0 μmol/L ,10 0 μmol/L ,5 0 0 μmol/L ,1mmol/L)能剂量依赖地减轻Aβ2 5-3 5的细胞毒性。结论 SF能够对抗Aβ2 5-3 5诱导的培养皮层神经细胞的损伤。Objective To study the protective effects of Sodium Ferulate (SF) on the damage of primarily cultured neurocyte introduced by A β 25-35 . Methods Put the cerebral cortex neurocyte of 17~18d fetal rats under the microscope through which we observe the morphologic changes of the neurocyte.The viability of the neurocyte was evaluated by MTT assay,LDH efflux was used to show damage degree of the membrane and MDA production to evaluate the hyper-oxidation of the PUFA. Results Treatment of primary cultured neurons with A β 25-35 (20μmol/L)for 24h caused a significant decrease in neurocyte viability (P<0.01, compared with normal control). Cell shedding, synapse shortening could be observed obviously through microscope. MTT assay showed that of the neurons descended obviously compared to the control. The ratio of LDH efflux increased significantly and MDA production in culture medium (P<0.01). SF (10μmol/L,50μmol/L,100μmol/L,500μmol/L, 1mmol/L) reduced the neurotoxicity induced by A β 25-35. Conclusions SF can concentration-dependently rescue cultured neurons from the injury caused by A β 25-35.
关 键 词:皮层神经细胞 阿魏酸钠 Β淀粉样蛋白25-35 自由基
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