缺血后适应对脑缺血树鼩海马TLR4表达的影响  

Postconditioning modulates TLR4 expression in hippocampus of tree shrews with thrombotic cerebral ischemia

作　　者：冯蕊[1,2] 李树清[2] 

机构地区：[1]昆明医学院第一附属医院风湿免疫科,云南昆明650031 [2]昆明医学院病理生理学教研室,云南昆明650031

出　　处：《中国病理生理杂志》2011年第6期1048-1052,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30971171);教育部博士点专项基金资助项目(No.20050678008);云南省教育厅科研基金资助项目(No.09Y0154)

摘　　要：目的:观察血栓性脑缺血树鼩海马Toll样受体4(TLR4)表达的改变,进一步探讨缺血后适应对海马TLR4表达的影响。方法:用光化学法建立血栓性脑缺血模型;并于缺血4 h夹闭缺血侧颈总动脉5 min,再通5min,重复3个循环,实施后适应处理。用HE染色观察海马组织学改变,Western blotting测定海马TLR4蛋白表达,RT-PCR测定海马TLR4 mRNA。结果:脑缺血4、24、72 h海马神经元损伤进行性加重,24h达高峰,后适应后损伤减轻。脑缺血海马TLR4蛋白表达明显增强(P<0.05)。与脑缺血组比较,后适应4h及24h TLR4蛋白表达减少(P<0.05),后适应72h TLR4蛋白表达增加(P<0.05)。海马TLR4 mRNA的表达趋势与蛋白表达基本一致。结论:脑缺血时海马TLR4表达明显增强,缺血后适应的脑保护机制可能与调控TLR4表达有关。AIM：To observe the effects of thrombotic cerebral ischemia and postconditioning on the expression of toll-like receptor 4（TLR4） in hippocampus of tree shrews.METHODS： The model of thrombotic focal cerebral ischemia was established by photochemical reaction.Four hours after the onset of photochemical reaction,ischemic postconditioning was induced by 3 repeated cycles of carotid artery occlusion for 5 min and reperfusion for 5 min.The histological changes of hippocampus（by HE staining）,TLR4 protein level（by Western blotting） and TLR4 mRNA expression（by semiquantitative RT-PCR） were observed.RESULTS： The extensive neuronal degeneration in hippocampus was observed from 4 h to 72 h and peaked at 24 h after cerebral ischemia,but was significantly attenuated after postconditioning.Cerebral ischemia caused a progressive increase in the expression of TLR4 protein at 4!h and 24 h（P0.05）,and decreased at 72 h（P0.05）.In contrast to ischemia groups,postconditioning decreased the expression of TLR4 protein at 4 h and 24 h（P0.05）,but an increase in the expression of TLR4 at 72 h（P0.05） was observed.Simultaneously,the level of TLR4 mRNA in hippocampus showed the tendency of approximate variation in accordance with the protein expression.CONCLUSION： The expression of TLR4 increases by cerebral ischemia.The protection mechanisms of postconditioning may be associated with modulating TLR4 expression.

关 键 词：脑缺血 TOLL样受体4 缺血后适应 海马 树鼩 

分 类 号：R363[医药卫生—病理学]