目的:观察加减地黄饮子对β-淀粉样蛋白1-40(Aβ-1-40)诱导的AD模型大鼠学习记忆障碍的改善作用及对胆碱乙酰化转移酶(choline acetyltransferase,ChAT)表达的影响。方法:采用大鼠海马立体定向注射凝聚态Aβ-1-40诱导老年性痴呆(Alzheimer's disease,AD)动物模型。采用Morris水迷宫测试大鼠寻找平台所需时间和通过原平台次数评价大鼠学习记忆能力及加减地黄饮子的干预作用。采用免疫组织化学染色法和计算机图像分析技术测定海马区ChAT表达。结果:模型组大鼠在定位航行试验中寻找隐匿平台平均逃避潜伏期较正常组显著延长,空间探索试验中跨越原平台位置次数明显减少(P〈0.01),加减地黄饮子组平均逃避潜伏期较模型组显著缩短,跨越原平台位置次数明显增加(P〈0.01),但多奈哌齐组和加减地黄饮子组比较差异无显著性(P〉0.05)。免疫组化实验结果显示,与假手术组比较,模型组大鼠海马区ChAT蛋白表达下降(P〈0.01)。与模型组比较,加减地黄饮子组ChAT蛋白表达升高(P〈0.01)。结论:加减地黄饮子对AD模型大鼠的学习记忆功能减退具有改善作用,可能与增强海马神经元ChAT表达,进而使Ach的合成增加有关。
Objective :To observe the effects of Modified Decoction of Rehmanniae on learning and memory ability in Alzheimer's disease (AD)rats induced by amyloid -β1-40 injection into brain and its mechanism. Methods : AD model in rats was incuced by amyloid - β1-40 sterotaxis injection the bilateral Hippocampus, Modified Decoction of Rehmanniae was given by oral administration for 28 days. The learning and memory ability of rats were evaluated with a series of tasks to find a hidden platform in Morris Water Maze. The expression levels of ChAT protein in the hippocampus were measured by immunohistochemical SABC techniques. Results :On the 2nd,3rd,4th,5 th days of place navigation test, the mean escape latencies of the model group were obviously increased compared with blank control group ( P 〈 0.01 ). In spatial probe test, the frequency of passing through the platform of the model group were obviously decreased as compared with the blank control group( P 〈0.01 ). On the 2nd,3rd, 4th,5th days of place navigation test, the mean escape latencies of the Modified Decoction of Rehmanniae were obviously decreased as compared with model group( P 〈0.01 ). In spatial probe test, the frequency of passing through the platform of the Modified Decoction of Rehmanniae were obviously increased as compared with the model. The ChAT protein expression was promoted in Modified Decoction of Rehmanniae groups compared with the model group. Conclusions : Modified Decoction of Reh- manniae has an effect of improving learning and ability of AD rats induced by amyloid - β1-40 injection the bilateral Hippocampus, which is possibly due to the promoting expression of ChAT protein.