摘要
目的研究微管结合蛋白-2(MAP-2)在慢性前脑缺血致血管性痴呆大鼠额、颞叶皮质和海马区的经时变化。方法采用双侧颈总动脉永久结扎方法制备慢性前脑缺血致VD大鼠动物模型;采用免疫组织化学方法检测痴呆鼠不同脑区MAP-2的经时变化情况;采用同济大学研制的HPIAS-1000高清晰彩色病理图文分析系统对不同脑区MAP-2阳性信号的面积密度进行分析。结果实验发现痴呆大鼠不同脑区MAP-2的表达随时间变化。缺血1个月、2个月、4个月后MAP-2的表达阳性面积逐渐减少,与对照组相比有统计学意义。从形态学变化角度来说,1个月时MAP-2轻度变化,提示为可逆性损伤。随着缺血时间的延长,MAP-2免疫组化染色越来越淡。至4个月时,MAP-2免疫组化染色基本消失,提示为不可逆损伤。结论慢性持续性脑血流量下降致MAP-2的改变在VD的病理生理过程中起重要作用。
Objective To study the duration changes of MAP-2 on the frontal cortex,temporal lobe and hippocampus of vascular dementia (VD) rats after chronic ischemia.Methods We established a VD rat model after chronic cerebral hypoperfusion by permanent bilateral common carotid arteries (CCA) occlusion.The changes of MAP-2 were observed by the immunohistochemical methods.The abnormalities of them were quantified with an image-analysis system.Results MAP-2 expression in different cerebral regions of VD rats was changes with time.There was a gradual decrease in number of MAP-2 in different cerebral regions after the occlusion of bilateral carotid arteries with the prolongation of ischemic time.But there was a slight change of the morphology of MAP-2 in the first month indicating that it might be reversible.With the prolongation of ischemic time,the change turned to inreversible.Conclusion The chronic and steady reduction of rCBF can bring out the decrease in number of MAP-2 in different cerebral regions.The changes of MAP-2 play an important role in the pathophysiological mechanism of vascular dementia.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2010年第10期879-881,共3页
Journal of Apoplexy and Nervous Diseases