摘要
目的探讨缺血再灌注对大鼠认知功能的损伤机制及人参皂甙Rg2干预作用。方法制备大鼠脑中动脉阻断法缺血再灌注模型，缺血60min后再灌注24h。用Morris水迷宫方法测定大鼠认知记忆能力变化；用免疫组织化学和图像分析方法检测脑组织B淀粉样蛋白（Aβ1-40）、其前体蛋白（APP）和NMDA受体蛋白（NR1）的表达。结果人参皂甙Rg22．5～10mg／kg及尼莫地平50wg／kg，使逃避潜伏期明显缩短（P〈0．01）；Aβ1-40及APP、NR1表达减弱（P〈0．05，0．01）。结论缺血再灌注可以通过上调β淀粉样蛋白（Aβ1-40）、其前体蛋白（APP）和NMDA受体蛋白（NR1）而引起认知功能障碍，人参皂甙Rg2对认知功能有保护作用。
Objective To investigate the impaired mechanism of cognitive handicap induced by ischemia reperfusion and the intervention of ginsenoside Rg2 in rats. Methods Ischemia reperfusion model was prepared by middle cerebral artery occlusion （MCAO）-reperfusion method. Reperfusion was performed 60 min after ischemia and persisted till 24 hours. Morris water maze was applied to analyze the changes in learning and memory abilities. Expressions of β amyloid, amyloid precursor protein and NMDA receptor protein（ NR1 ） were detected with immunohistochemistry and image analysis. Results The escaping incubation period was prolonged 24h after ischemia-reperfusion in rats （model group） , while the period was shorten in ginsenoside Rg2 group and nimodipine group compared with the model group（ P 〈 0.01 ）. Expressions of β amyloid, amyloid precursor protein and NMDA receptor protein NR1 were increased in model group, the expressions were decreased in ginsenoside Rg2 groups and Nimodipine group compared with the model group（ P 〈0.05,0.01 ）. Conclusion Isehemia reperfusion could cause cognitive handicap through up-regulation of β amyloid, amyloid precursor protein and NR1 and ginsenoside Rg2 has protective effect on cognitive function in rats.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2008年第4期417-420,共4页
Journal of Apoplexy and Nervous Diseases
基金
国家科技部生命研究中心重大产业开发资助(96-901-01-12A)
