【摘要】 目的观察脑缺血对阿尔茨海默病转基因鼠记忆功能的影响。方法选用3月龄携带突变淀粉前体蛋白(APP)基因和早老素-1(PS1)基因的转基因鼠与非转基因鼠,应用光化学法诱导脑梗死形成并将转基因鼠与非转基因鼠分别分为脑缺血组和假手术组,以TFC方法测定脑梗死体积,应用Morris水迷宫试验测定记忆功能。结果梗死后第7 d APP/PS1转基因鼠总梗死体积和皮层梗死体积显著大于非转基因鼠(n=6,P＜0．01);与假手术组相比,缺血组APP/PS1转基因鼠在梗死后第4 d逃避潜伏期显著延长(P＜0．01),在梗死后第7 d目标象限游泳时间显著缩短(P＜0．05);缺血组非转基因鼠上述两项指标均无显著变化。人为地将非转基因鼠分为大梗死体积非转基因鼠组和小梗死体积非转基因鼠组,梗死体积相似的APP/PS1转基因鼠组和大梗死体积非转基因鼠组记忆功能间差别有显著性意义(P＜0．05)。结论脑缺血促进APP/PS1转基因鼠记忆障碍提早发生。其机制与梗死体积无关。更多还原

【Abstract】 Objective To investigate the effect of cerebral ischemia on the memory function in the mice carrying mu- tant amyloid precursor protein(APP)and precinilin-1(PS1)genes.Methods In 3 months old APP/PS1 mice and non- transgenic mice,photothrombotic stroke was induced and the transgenic mice and non-transgenic mice were divided into stroke group and sham group respectively,infarct volume was evaluated with TTC method on 7 days after cerebral ischemia,memory function was evaluated with Morris water maze from day 3 to day 7 after ischemia.Results Infarct volume and cortical infarct volume in the APP/PS1 mice was(8.750±0.611)% and(5.40±0.31)% respectively,higher than that in the non-transgen- ic mice(n=6,P＜0.01).Compared with the sham group,at the acquisition stage,latency to the hidden platform increased significantly from day 4 to day 6 after ischemia in the stroke group in the APP/PS1 mice,while did not increase in the non- transgenic mice;at the probe stage,time in the target quadrangle during 60 s reduced in the stroke group in the APP/PS1 mice (n=6,P＜0.05),while did not reduce in the non-transgenic mice.12 non-transgenic mice were divided artificially:large infarct volume group and small infarct volume group.Time in the target quadrangle in large infarct volume non-transgenic mice group was longer than that in the APP/PS1 mice group(P＜0.01),while there was no difference in infarct volume between these two mice groups(P＞0.05).Conclusion Cerebral ischemia accelerates memory impairment in the APP/PS1 transgenic mice.The increased infarct volume in the APP/PS1 transgenic mice doesn’t play a key role in the accelerated post-stroke mem- ory impairment.更多还原