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作 者:严家川[1] 蒋晓江[1] 邓娟[1] 王延江[1] 周华东[1]
机构地区:[1]第三军医大学大坪医院野战外科研究所神经内科,重庆400042
出 处:《重庆医学》2008年第7期686-687,690,共3页Chongqing medicine
基 金:重庆市自然科学基金计划项目(2005BB5276)
摘 要:目的探讨烟碱抗β-淀粉样蛋白(Aβ)神经毒性作用的机制。方法在海马神经组织细胞混合培养体系中分别加入烟碱、β-淀粉样蛋白,用MTT法、ELISA分别测定海马细胞增殖活性和培养细胞上清液中IL-1β含量。结果烟碱加Aβ组细胞增殖活性明显高于Aβ组。烟碱加Aβ组培养细胞上清液中IL-1β含量明显低于Aβ组。结论烟碱可抑制Aβ所致的IL-1β表达增加,对Aβ神经细胞毒性具有拮抗作用。Objective To explore the mechanism of nicotine against the neurotoxic effect of β-amyloid protein in the hippocampal cultures, Methods To establish the mixed hippoeampal cultures,then the hippocampal cultures incubated with nicotine and β-amyloid protein,or with β-amyloid protein alone respectively. MTT and ELISA were adopted to estimate the cell viability and the levels of IL-1β of the culture supernatants. Results The cell viability of nicotine groups were higher than β-amyloid protein group. The levels of IL-1β in nicotine groups were decreased compared with the β-amyloid protein group. Conclusion Nicotine could inhibit the increase of IL-1β induced by Aβ protein,and against the neurotoxic effect of Aβ.
分 类 号:R749.16[医药卫生—神经病学与精神病学]
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