TrkA和Bcl-2在局灶性脑缺血再灌注大鼠大脑皮质中的表达  

Expression of TrkA and Bcl-2 in cerebral ischemic/reperfusion rats

作　　者：杨杰[1] 周芝文[1] 郑丽君[1] 曾进[1] 杨期东[1] 

机构地区：[1]中南大学湘雅医院神经内科,湖南长沙410008

出　　处：《中风与神经疾病杂志》2010年第7期584-588,共5页Journal of Apoplexy and Nervous Diseases

基　　金：湖南省科学技术厅科技计划资助项目(05SK3003)

摘　　要：目的探讨局灶性脑缺血再灌损伤后TrkA与Bcl-2基因/蛋白的表达变化。方法 250～350g健康雄性SD大鼠48只,分为对照组(n=24)和脑缺血模型组(n=24)。线栓法制备大脑中动脉栓塞模型,分别在再灌注后6h、24h、48h、7d共4个时间点处死大鼠。运用原位杂交及免疫组化法检测TrkA、Bcl-2基因/蛋白表达变化。结果与对照组相比,模型组TrkA、Bcl-2基因/蛋白阳性表达明显增加,差异有统计学意义(P<0.01)。结论大鼠脑缺血再灌注损伤后,可能通过上调TrkA和Bcl-2的表达,起到神经保护作用。Objective The mRNA and protein expression of TrkA and Bcl-2 in MCAO rats were studied. Methods The healthy male Sprague-Dawley rats weighting 250～350g were randomly divided into two groups：a control group （n=24） and an ischemia/reperfusion （I/R） group （n=24）. Transient focal cerebral ischemia was induced by middle cerebral artery occlusion （MCAO）. The mRNA and protein expression of TrkA and Bcl-2 were measured with methods of immunohistochemistry and in situ hybridization respectively. Results Compared with the control group,the mRNA and protein expression of TrkA and Bcl-2 in I/R group increased significantly. Conclusion The mRNA and protein expression of TrkA and Bcl-2 might increase after cerebral ischemia/reperfusion which might protect the neurons.

关 键 词：脑缺血 TRKA BCL-2 

分 类 号：R743.3[医药卫生—神经病学与精神病学]