丁苯酞可提高低氧低糖后前脑神经元线粒体轴浆运输及末梢乙酰胆碱释放的实验研究  

Experimental study on N-Butylphthalide in Increasing the Mitochondrial Axonal Transport and the Acetylcholine Release of Forebrain Neurons after Hypoxia and Hypoglycemia

作　　者：张颖影 国敏 王颖喆 赵鸿琛 崔梅 Zhang Yingying;Guo Min;Wang Yingzhe;Zhao Hongchen;Cui Mei(Department of Neurology,Huashan Hospital Affiliatedto Fudan University,Shanghai,200040,P.R.China)

机构地区：[1]复旦大学附属华山医院神经内科,上海200040

出　　处：《老年医学与保健》2018年第4期372-375,385,共5页Geriatrics & Health Care

基　　金：国家自然科学基金(81471173;81571109);上海市科学技术委员会引导项目(16411970200)

摘　　要：目的观察丁苯酞(N-butylphthalide,NBP)对低氧低糖刺激的前脑神经元线粒体轴浆运输的作用以及对轴突末梢乙酰胆碱释放的影响。方法体外培养前脑神经元,分为对照组、低氧低糖组和低氧低糖+NBP组,利用活细胞工作站测定不同组神经元轴突内线粒体轴浆运输,高效液相色谱检测乙酰胆碱水平;Western blot检测线粒体转运相关调控蛋白Milton及Miro表达。结果与对照组相比,低氧低糖组神经元轴浆正、反向线粒体运输比例下降(P<0.05),乙酰胆碱递质释放和线粒体转运相关调控蛋白Milton及Miro表达水平亦下降(P<0.05),低氧低糖+NBP组有效改善了低氧低糖组上述指标的下降(P<0.05)。结论丁苯酞可改善低氧低糖状况下神经元的线粒体轴浆运输及轴突末梢乙酰胆碱能释放,这一作用可能是通过增加线粒体转运相关调控蛋白Milton及Miro表达实现的。Objective To observe the effect of N-Butylphthalide on the axonal transport of mitochondria and on the release of acetylcholine at axonal terminals of the forebrain neurons after hypoxia and hypoglycemia. Methods The forebrain neurons were cultured in vitro and divided into 3 groups： control group, hypoxia-hypoglycemia group and hypoxia-hypoglycemia plus N-Butylphthalide group; the mitochondrial axonal transport in each group was measured by living cell workstation; the level of acetylcholine was detected by high performance liquid chromatography（HPLC）; the expressions of mitochondrial transport related regulatory proteins Milton and Miro were detected by Western blot. Results The proportions of anterograde and retrograde mitochondrial axonal transport in hypoxia-hypoglycemia group were significantly smaller than those in control group（P0.05） and the release of acetylcholine transmitters and the expression level of mitochondrial transport related regulatory proteins Milton and Miro decreased much more（P0.05）; better improvement in the decrease of above indicators was found in hypoxia-hypoglycemia plus N-Butylphthalide group than in hypoxia-hypoglycemia group（P0.05）. Conclusions N-Butylphthalide can improve the mitochondrial axonal transport and the release of acetylcholine at the axon end of neurons after hypoxia and hypoglycemia, which may be of certain relationship with the expression increase of mitochondrial transport related resgulatory proteins Milton and Miro.

关 键 词：丁苯酞 脑缺血 低氧低糖 线粒体 轴浆运输 

分 类 号：R338[医药卫生—人体生理学]