大鼠局灶脑缺血酪氨酸激酶B表达图像分析

目的 观察局灶脑缺血大鼠酪氨酸酶B(TrkB)阳性神经元的表达,探讨脑缺血损伤与TrkB的关系。方法 制作大鼠局灶脑缺血模型,应用免疫组化方法观察不同缺血时间、不同脑区TrkB阳性神经元数的动态改变,并进行图像分析。结果 正常脑组织内即存在着一定数量的TrkB阳性神经元,脑缺血损伤后,在额、顶叶皮质及尾壳核外侧部的变性坏死区中心,TrkB阳性神经元缺失,而变性坏死区周边的半暗带区TrkB阳性神经元自缺血6h开始明显增多,且持续于整个缺血期。其它部位TrkB表达也不同程度增强。方差分析显示,与正常对照组比较,除假手术组外(P>O.05).缺血组各组均差异显著(P<0.01)。结论 脑缺血损伤后TrkB的表达有显著改变,考虑与神经元的损伤修复机制有关。

The picture analysis of expression of tyrosine kinase B after focal cerebral ischemia in rats

Objective To observe the expression of tyrosine kinase B (TrkB) after focal cerebral ischemia in rats, and to study the relationship between cerebral ischemia insult and ryrosine kinase B. Methods The model of focal cerebral ischemia in rats was set up. Dynamic changes of TrkB positive neurons number in different cerebral regions at different time were observed with method of immunohistochemistry, and the picture analysis was applied. Results There was a certain number of TrkB positive neurons in the normal brain. After ischemia, the TrkB positive neurons diappeared in the center of necrotsis in the frontal and parietal cortex and the outside of caudatoputamen. But the TrkB positive neurons around the necrotic area obviously increased after 6 hours of ischemia, and kept higher through whole ischemic phrase. In other areas, the expression of TrkB was also increased to different degrees. The bivariate analysis displayed that there was significant difference between the control group and every ischemia group (P<0. 01), and there was no significant difference between the control group and the sham-operated group (P>0. 05). Conclusion After the attack of cerebral ischemia, the expression of TrkB has significant changes. The changes are regarded to be related to the mechanism of neuronic injury and repair-ment