人参皂甙Rb1对阿尔茨海默病大鼠海马结构β-淀粉样蛋白表达的影响

EFFECT OF GINSENOSIDE Rb1 ON β-AMYLOID PROTEIN OF HIPPOCAMPAL FORMATION IN ALZHEIMER'S DISEASE MODEL RATS

目的观察人参皂甙Rb1对阿尔茨海默病(AD)模型大鼠学习记忆能力及海马结构β-淀粉样蛋白表达的影响。方法动物分3组:对照组、模型组及治疗组,用D-半乳糖联合三氯化铝建立AD大鼠模型,治疗组在造模后给予人参皂甙Rb1腹腔注射4周;采用Morris水迷宫测试大鼠的空间学习记忆能力,用免疫组织化学方法观察海马结构β-淀粉样蛋白的表达。结果与对照组相比,模型组大鼠各时间段的逃避潜伏期均显著延长(P<0.01),海马CA1、CA3区及齿状回β-淀粉样蛋白表达的阳性细胞数明显增多(P<0.01);治疗组大鼠的逃避潜伏期较模型组明显缩短(P<0.01),海马CA1、CA3区及齿状回的β-淀粉样蛋白阳性细胞数显著减少(P<0.01)。结论人参皂甙Rb1对AD模型大鼠学习记忆损害具有明显改善作用,其机制可能与人参皂甙Rb1减少海马结构β-淀粉样蛋白的表达有关。

Objective To observe the effect of ginsenoside Rbl on the learning and memory and the changes in beta-amyloid expression of hippocampal formation in Alzheimer＇s disease （AD） model rats. Methods The rats were divided into control group, AD group and ginsenoside Rb1-treated group. The AD model was treated with D-galactose and aluminium tricbloride. Ginsenoside Rb1 was given to the treated group after the establishment of AD model. Morris water maze for testing learning and remembrance ability of rats was used. Immunobistocbemical staining for beta-amyloid was performed. Results The escape latency at all time segments of the model group was signifticantly prolonged than that of the control group （P〈0. 01）. The number of beta-amyloid positive cells in each hippocampal subregion of the model group increased strikingly （P〈0.05, P〈0.01） . The escape latency of the treated group was significantly shortened compared with that of the model group （P〈0. 01） . The number of beta-amyloid positive cells of hippocampal CA1. CA3 and gyrus dentatus in the treated group was obviously decreased （P〈0.01） . Conclusion The learning and memory impairment of AD model rats was obviously improved by ginsenoside Rbl. The mechanism may be the decrease of beta-amyloid expression in hippocampal formation after ginsenoside Rbl treatment.