局灶脑缺血大鼠脑源性神经营养因子及其受体的表达  

Expression of Brain-Derived Neurotrophic Factor and TrkB After Focal Cerebral Ischemia in Rats

作　　者：王佩[1] 齐浩波 乔占涛 王淑敏[1] 李育臣[2] 

机构地区：[1]河北省保定市第四医院神经内科 [2]河北医科大学第三医院神经内科

出　　处：《中西医结合心脑血管病杂志》2003年第3期138-140,共3页Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease

摘　　要：目的 :探讨脑缺血损伤与脑源性神经营养因子 (BD NF)及其受体TrkB之间的关系。方法 :用线栓法制备大鼠脑缺血模型 ,采用免疫组织化学方法及图像分析测定不同缺血时间额叶和顶叶BDNF及TrkB阳性神经元数目。结果 :与假手术组相比 ,在额叶BD NF及TrkB阳性神经元数目于缺血 6h开始增加 (P <0 .0 5) ,缺血 3d达到高峰 (P <0 .0 0 1 ) ,缺血 7d降至正常水平(P >0 .0 5) ;在顶叶BDNF及TrkB阳性神经元数目于整个缺血过程均明显增加 (P <0 .0 0 1 )。结论 :脑缺血损伤后 ,BDNF和TrkB表达同时增强 ,可能对脑缺血损伤有保护作用。Objective:To explore the relationship between the cerebral ischemic insult and Brain-derived neurotrophic factor and its recepter TrkB.Methods:The model of focal cerebral ischemia was set up by blocking up the middle cerebral artery(MCA)with filament in rats. The expression of BDNF and TrkB positive neurons in frontal cortex and parietal cortex of different time was observed with the method of immunocytochemistry and the picturical analysis system.Results:Compared with the sham group, the number of BDNF and TrkB positive neurons in frontal cortex increased after 6 hours(P<0.05), and increased remarkably after 3rd day(P<0.001), At 7th day decreased to normal level (P>0.05). In parietal cortex, the number of BDNF and TrkB positive cells remained very high in the whole ischemic process (P<0.001). Conclusion:The expression of BDNF and TrkB increased at the same time after ischemia to protect neurons in frontal cortex and parietal cortex.

关 键 词：脑缺血损伤 脑源性神经营养因子 受体 免疫组织化学 

分 类 号：R741.02[医药卫生—神经病学与精神病学]