海马神经元缺血/再灌注后自噬的表达及其作用  

Expression and function of autophagy after ischemia/reperfusion in rats hippocampus neuron

作　　者：苏方[1] 张培[1] 姜治伟[1] 彭德清[1] 高璐滢[1] 刘书琴[1] 钱令波[1] 叶治国[1] 夏强[1] 

机构地区：[1]浙江大学医学院生理学系,杭州310058

出　　处：《中国应用生理学杂志》2011年第2期187-191,共5页Chinese Journal of Applied Physiology

基　　金：浙江省自然科学基金资助项目(Y206179);浙江大学医学院第12期SRTP

摘　　要：目的:研究自噬在大鼠海马神经元缺血缺氧/再灌注过程中的表达及自噬在神经元缺血缺氧/再灌注损伤中的作用。方法:原代培养的大鼠海马神经元经2 h的氧糖剥夺和不同时段的再灌注处理,MTT法检测细胞活性,透射电镜下检测自噬的特异性结构,免疫荧光化学法检测自噬特异性蛋白微管相关蛋白1轻链3(LC3B)的表达。应用自噬抑制剂3-甲基腺嘌呤(3-MA)检测神经元的活性。结果:经氧糖剥夺/再灌注后,海马神经元的活性比未经氧糖剥夺/再灌注组显著地降低。透射电镜和免疫荧光检测,未经氧糖剥夺/再灌注的神经元自噬的发生率极低,氧糖剥夺后和再灌注的不同时间段,均有自噬的发生。应用自噬抑制剂3-MA阻断自噬后,神经元的存活率显著降低。结论:缺血缺氧/再灌注能激活海马神经元的自噬,并可能在缺血缺氧/再灌注过程中起对抗损伤的作用。Objective：To explore the expression of autophagy after ischemia/reperfusion and its possible function in rats hippocampus neurons.Methods：After 2 hours oxygen-glucose deprivation and different periods time of reperfusion（OGD/R） treatment in primary cultured hippocampal neurons,neuron viability was evaluated by MTT assay,specific structure of autophagosome and specific protein of autophagy microtubule-associated protein 1 light chain 3 B（LC3B） were detected by transmission electron microscope and immunofluorescence respectively.The inhibitor of autophagy 3-Methyladenine（3-MA） was also used to exam the viability of neurons.Results：Treatment by OGD/R markedly reduced neuronal viability.Compared to the control group,autophagy existed in different time periods after OGD/R shown both in transmission electron microscope and immunofluorescence.Application of 3-MA significantly reduced neuronal viability.Conclusion：Oxygen-glucose deprivation can activate autophagy in rat hippocampus neurons,which may resist the injury during ischemia/reperfusion.

关 键 词：自噬 神经元 缺血/再灌注 

分 类 号：R338.2[医药卫生—人体生理学]