|
全脑缺血再灌注大鼠小脑NGF BDNF的表达 |
| |
李爱丽 关文明 王彦红 石育原
摘 要 目的：探讨老龄大鼠全脑缺血再灌注损伤对小脑NGF、BDNF 表达的 影响。方法：采用Pulsinelli-Brierley4血管阻塞法进行改良制作全 脑缺血再灌注 动物模型，通过免疫组化方法对小脑NGF、BDNF的表达进行动态观察。结果：缺血 再灌注损伤时，小脑分子层、颗粒层和髓质出现一过性NGF表达，而梨状细胞层NGF表达呈持 续性；小脑分子层和梨状细胞层始终无BDNF表达，颗粒层的BDNF表达量无变化，但 髓质BDNF表达量出现增加现象。结论：小脑对缺血再灌注损伤具有短 暂的 NGF保护作用，分子层和梨状细胞层不存在BDNF保护机制，而髓质具有良好的BDNF保护机制 。
关键词 老龄大鼠 缺血再灌注 神经生长因子 脑源性神经营养因子
中国图书分类号 R743.3
Expressions of NGF and BDNF in cerebellum area s after whole brain ischemia/reperfusion in senile Wistar rats
LI Ai-Li GUAN Wen-Ming WANG Yan-Hong
（Dept. of Neurology, Sec ond Teaching Hospital Bethune University of Medical Sciences, Changchun 130041）
Abstract Objective:To explore the effects of NGF a nd BDNF on cerebellum after ischemia/reperfusion in senile Wistar rats.Methods:The animal model of whole brain ischemia/reperfusion was m a de with improved method of bloching four-vessel of Pulsinelli-Brierley's.The d yn amic changes of expressions of NGF and BDNF in cerebellum were observed with imm unocytochemistry method.Results:There appeared a transient NGF expression in molecular, granular layers and medulla area ischemia reperfusi on h ppened, but persistent expression in Purkinje layer. There were no BDNF expressi ons in molecular and Prukinje layers, no expression change in granular layer, bu t rich expression in medulla after ischemia/reperfusion.The peak level of BDNF w a s observed in medulla of cerebellum.Conclusion:There was a transient protective action of NGF in cerebellum to ischemia/reperfusion, no pr otective action of BDNF in molecular and Purkinje layers,but well protectire act ion in medulla.
Key words Senile rat Ischemia/reperfusion NGF BDNF
神经营养因子(neurotrophic factors,NTFs)是近年来引起科学家们非常关 注的特异蛋白质分子［1］，NTFs有许多种类，神经生长因子(nerve growth factor, NGF)和 脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)是其中的2种。本文选 用Wistar老龄大鼠制作全脑缺血再灌注动物模型，采用免疫组化方法对缺血 小脑不同结构NGF、BDNF的表达进行动态观察，以揭示全脑缺血再灌注损伤后小脑 NGF、BD[1] [2] [3] 下一页
上一个医学论文： APA微囊对免疫细胞和细胞因子隔离效应的研究
下一个医学论文： 人类疱疹病毒6 7型体外感染淋巴细胞对CD抗原表达的影响
|
|
|
|
|
|
|
您现在的位置： 绿色健康网 >> 医学论文 >> 基础医学论文 >> 正文