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机构地区:[1]民航总医院神经内科,北京100123 [2]吉林大学白求恩第一医院神经内科,吉林长春130021
出 处:《中风与神经疾病杂志》2015年第3期201-204,共4页Journal of Apoplexy and Nervous Diseases
摘 要:目的研究神经丝蛋白200(NF200)在慢性前脑缺血致血管性痴呆大鼠额、颞叶皮质和皮质下白质的经时变化。方法采用双侧颈总动脉永久结扎方法制备慢性前脑缺血动物模型;采用免疫组织化学方法检测痴呆鼠不同脑区NF200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NF200阳性信号的面积密度进行分析。结果实验发现双侧颈总动脉永久结扎后不同脑区NF200的表达随时间变化。缺血1 m,2 m,4 m后NF200的表达阳性面积逐渐减少,与对照组相比有统计学意义。在形态学变化方面,1 m时NF200轻度变化,提示为可逆性损伤。随着缺血时间的延长,NF200免疫组化染色越来越淡。至4 m时,NF200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NF200的改变在血管性痴呆的病理生理过程中起一定作用。Objective To study the duration changes of NF200 on the frontal cortex,temporal lobe and callosum of vascular dementia( VD) rats after chronic ischemia. Methods We established a VD rat model after chronic cerebral hypoperfusion caused by permanent bilateral common carotid arteries( CCA) occlusion. The changes of NF200 by the immunohistochemical methods were observed. The abnormalities of them were quantified with an image-analysis system. Results NF200 expression in different cerebral regions of VD rats was changesd with time. there was a gradual decrease in number of NF200 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 NF200 in the first month indicating that it was reversible. With the prolongation of ischemic time,the change turned to be inreversible. Conclusion The chronic and steady reduction of r CBF can bring out the decrease in number of NF200 in different cerebral regions. The changes of NF200 played an important role in the pathophysiological mechanism of vascular dementia.
分 类 号:R743[医药卫生—神经病学与精神病学]
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