摘要
目的观察血管性痴呆(VD)小鼠海马中细胞外信号调节激酶(ERK2、p-ERK)的表达变化,探讨其在VD发病中的作用机制。方法采用双侧颈总动脉反复缺血-再灌注法制备小鼠VD模型,设立假手术组作为对照。术后第29、30天,经跳台试验和水迷宫试验对各组小鼠进行行为学成绩测试,用免疫组化方法观察各组小鼠海马CA1区ERK2及海马CA3区p-ERK的表达变化。结果VD模型小鼠学习、记忆成绩较假手术组显著下降(P<0.05);模型组小鼠海马CA1区ERK2的表达及海马CA3区p-ERK的表达较假手术组减少,差异有统计学意义(P<0.05)。结论海马神经元内ERK的表达减少可能参与了血管性痴呆的发病机制,因此应用能促进ERK表达的药物可能成为治疗VD的有效方法之一。
Objective To observe the expressing features of extracellular signal--regulated kinase (ERK2 and p--ERK) in the hippocampus of mice with vascular dementia(VD), and explore its role in the pathogenesis of VD. Methods The models of VD mice were established by three times ischemia-- reperfusion of bilateral common carotid arteries, sham group was set up as contrast group. The behavioral scores of all mice from two groups were investigated by step--down test and water maze test at days 29, 30 respectively. The expressing features of ERK2 in hippocampus CA1 and p-ERK in hippoeampus CA3 were observed by immunohistochemistry technique. Results The grades of learning and memory of VD mice were obviously decreased compared with sham group (P 〈 0.05) . The expression of ERK2 in hippocampus CA1 and p-ERK in hippocampus CA3 was significantly lower in the model group than that in the sham group (P 〈 0.05) . Conclusions The decreased expression of ERK in hippocampal neurons might participate the pathogenesis of VD. It is suggested that the application of some drugs which could increase the concentration of ERK in hlppocampus might be benefit in treatment of VD.
出处
《神经疾病与精神卫生》
2007年第4期251-253,共3页
Journal of Neuroscience and Mental Health
基金
河北省自然科学基金资助项目(301415)
关键词
血管性痴呆
小鼠
细胞外信号调节激酶
免疫组化
海马
Vascular dementia
Mice
Extracellular signal--regulated kinase
Immunohistochemistry
Hippocampus