自噬标志性分子LC3B在大鼠全脑缺血复灌损伤中海马CA1区的表达及意义  

Expression of LC3B in rat hippocampal CA1 neurons after global cerebral ischemia-reperfusion

作　　者：曾斌[1] 王静文[1] 张玉琳[1] 任典寰[1] 应志国[1] 

机构地区：[1]宁波卫生职业技术学院人体形态教研室,浙江宁波315100

出　　处：《中国临床解剖学杂志》2012年第6期667-669,共3页Chinese Journal of Clinical Anatomy

基　　金：浙江省2010年度高校优秀青年教师资助计划(浙教办高科〔2010〕175号);浙江省教育厅科研项目(Y200906656)

摘　　要：目的探讨自噬标志分子LC3B在大鼠全脑缺血复灌不同时间的表达以及对海马神经元损伤的影响。方法采用四血管法(4-vessel-occlusion,4-VO)法制作大鼠全脑缺血模型,随机将33只SD大鼠分成假手术组和缺血再灌注组。在大鼠全脑缺血20 min后,分别恢复血流灌注30 min、1、2、4、6、8、12、24、48、72 h,用免疫组织化学法检测海马CA1区神经元LC3B的表达。结果 LC3B在大鼠全脑缺血20 min复灌2 h开始表达,在复灌12 h表达到达高峰,之后逐渐减弱。结论自噬的激活介导了大鼠全脑缺血再灌注海马CA1区神经元的损伤死亡,长时间脑缺血再灌注损伤中自噬激活的时间更早及介导神经元的损伤更严重。Objective To explore expression change of LC3B in hippocampus, and the hippocampal neuronal death after global cerebral ischemia/reperfusion in rats. Methods Transient global cerebral ischemia was induced by four-vessel occlusion method. The SD rats weighing 250-320 g were randomly divided into 2 groups： the sham-operated group and the ischemia/reperfusion group. The expression of LC3B was detected by immunohistochemistry analysis. Results The expression of LC3B in the ischemia/reperfusion group got increased after 2h of reperfusion, and the peak appeared at 12 h of reperfusion. Conclusions The occurred LC3B activation leads to the neuronal death of hippocampal CA1 induced by ischemia/reperfusion. The earlier high expression of LC3B occurred, the more severe neuronal death appeared after 20-rain global cerebral ischemia. These results suggest that autophagy pathway play a more harmful role in neuron death after long time ischemia.

关 键 词：全脑缺血 缺血再灌注损伤 自噬 LC3B/LC3-II 

分 类 号：R743[医药卫生—神经病学与精神病学]