Aβ_(1～42)致老年性痴呆大鼠海马神经元细胞外信号调节激酶1,2的表达

Expressions of ERK1 and ERK2 in the hippocampus of rats with Aβ_(1～42) injected model of Alzheimer disease

目的：建立老年性痴呆大鼠模型，观察老年性痴呆大鼠海马神经元细胞外信号调节激酶1，2表达的变化，探讨其在老年性痴呆发病机制中的作用。方法：采用立体定向下双侧海马注射Aβ1～42建立老年性痴呆动物模型，经Y型电迷宫试验测试其行为学，采用免疫组织化学、蛋白印迹等方法观察细胞外信号调节激酶1，2表达变化。结果：模型组大鼠学习记忆能力较对照组显著下降，免疫组化显示海马CA1区细胞外信号调节激酶1，2的免疫反应阳性神经元数目及细胞平均光密度值均显著减少，蛋白印迹显示模型组较对照组条带变细，灰度值变小，差异均有统计学意义（P〈0．05）。结论：海马神经元细胞外信号调节激酶1，2表达的减少可能参与了老年性痴呆的发病机制。

Objective To explore the roles of ERK1 and ERK2 in the pathogenesis of Alzheimer disease by establishing model of Alzheimer disease and observing the expressions of ERK1 and ERK2 in the hippocampus of Alzheimer disease rats. Methods Alzheimer disease model was established by injecting Aβ1～42 into the bilateral hippocampus of rats. The learning and memory abilities of action were studied with Y maze; the expressions of ERK1 and ERK2 in hippocampus CA1 were observed with immuno-histochemistry WB. Results Compared with control group, the abilities of learning and memory of Alzheimer disease rats obviously decreased; the numbers of ERK1 and ERK2 immunoreactive neurons within the hippocampus CA1 region in the model group were significantly lower; the band of ERK1 and ERK2 were thinner by WB in hippocampus in the model group （P〈0. 05）. Conclusion The decreased expression of ERK in hippocampal neurons might participate in the pathogenesis of Alzheimer disease.