慢性脑灌注不足大鼠海马cai区神经丝蛋白表达的 - 第三军医大学学报.doc

慢性脑灌注不足大鼠白质功能的变化 宁 宁，赵士福，成戎川，梁伟华 (第三军医大学新桥医院神经内科， 400037) 目的：研究慢性脑灌注不足时对大鼠的影响。方法：采用双侧颈总动脉结扎制作慢性脑灌注不足动物模型。不同时间潜伏期检查免疫组化检测神经丝蛋白（NF200）。结果：⑴术后半月组、术后1月组、术后2月组对照组大鼠下肢潜伏期进行性延长(P0.01)。⑵与对照组相比，神经丝蛋白NF200逐渐降低。结论： 关键词 慢性脑灌注不足；神经丝蛋白；；运动诱发电位ffect of whiter matter function in the rats with chronic cerebral hypoperfusion NING ning, ZHAO Shi-fu, CHENG rong-chuan, LIANG wei-hua (Department of Neurology, The Second Affiliated Hospital, The Third Military Medical University, Chongqing 400037) ABSTRACT Objective: To investigate effect of whiter matter function in the rats with chronic cerebral hypoperfusion .Methods: Experimental group were treated with a permanent bilateral occlusion of both common carotid arteries (2-VO) to establish chronic cerebral hypoperfusion model. Examinating latency with different time. Neurofilament protein（NF200）were carried out an experiment in immunohistochemistrical reaction. Results: ⑴2 weeks ,1 month and 2 months later after operation, latency was significantly delay in experimental group(P0.01) as compared with the control group.⑵Activity of NF200 in the sample rats was decrease . Conclusion: Axonal conduction and transmission were impact in chronic cerebral hypoperfusion. The delay of motor evoked potentials appear to extend the ischemic time with the trend of gradually extended.NF200 decreased expression was impact in axonal structure and transport function. Key words Chronic cerebral hypoperfusion ；eurofilament protein ；Immunohistochemistry；慢性脑灌注不足(chronic cerebral hypoperfusion，CCH)在老年个体中普遍存在，是导致老年期认知障碍和运动障碍主要原因，长期反复损害易导致血管性痴呆，而传导功能损害是其重要机制之一[1、 2 ]。既往人们认为白质对缺血具有很高的耐受性，但近年研究显示脑白质对慢性缺血缺氧的敏感性远高于皮质，特别是富含髓鞘的白质，易引起脱髓鞘导致轴突的不可逆损害。神经丝蛋白NF200 的变化情况，阐明其病理生理机制，为临床上防治由慢性脑灌注不足引起的痴呆提供理论依据。1 材料和方法 1.1 材料 1.1.1 主要试剂 小鼠抗大鼠磷酸化NF200单抗购自武汉博士德生化试剂公司，免疫组化染色SP试剂盒及DAB染色试剂盒购自北京中杉生化试剂公司1.1.2 实验动物及分组 选用纯种健康Sprague-Dawley(SD)大鼠24只(第三军医大学大坪医院野战外科研究所实验动物中心提供)，2~3月龄，雌雄不，体重200~250g。大鼠随机分为对照组(n=6)、缺血半月组(n=6)、缺血1月组(n=6)和缺血2月组(n=6)。 1.2 1.2.1模型制备 我们采用大鼠持久双侧颈总动脉结