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目的:观察复方中药脑尔康对慢性铝中毒阿尔茨海默病(AD)模型小鼠学习记忆及脑内淀粉样前体蛋白(APP),β淀粉样蛋白(Aβ)表达的影响,探讨该药抗痴呆的分子机制。方法:60只昆明小鼠随机分为空白对照、模型、西药吡啦西坦、脑尔康高、中、低剂量6组,除空白组外,其余各组均采用氯化铝(AlCl3)溶液以100 mg.kg-1ip造模,空白组给予等量生理盐水ip,3个剂量脑尔康组给予脑尔康(34,17,8.5 g.kg-1.d-1)连续ig 50 d,吡啦西坦组给予吡啦西坦(10 g.L-1)ig,空白组和模型组给予等量生理盐水ig。采用跳台法检测AD模型小鼠学习记忆成绩,用免疫组织化学方法观察脑尔康对AD模型小鼠脑皮层及海马结构区域APP,Aβ表达的影响,对APP,Aβ阳性反应物质采用图像信号采集与分析系统进行灰度分析。结果:与对照组比较,模型组记忆潜伏期明显缩短(P<0.01),学习潜伏期明显延长(P<0.05),学习与记忆的错误次数明显增多(P<0.01);用药各组分别与模型组比较记忆潜伏期明显延长(P<0.01),学习潜伏期明显缩短(P<0.05),学习与记忆的错误次数明显减少(P<0.01)。各用药组模型小鼠脑内APP,Aβ的表达均不同程度减少(P<0.05或P<0.01);脑尔康3个剂量组比较存在明显量效关系。结论:脑尔康对慢性铝中毒AD模型具有显著的抗痴呆作用,其作用机制可能与调控APP,Aβ表达有关。
Objective: To observe the effect of compound Chinese medicine Er Kang on the learning and memory and the expression of amyloid precursor protein (APP) and amyloid β (Aβ) in mice with chronic Alzheimer’s disease (AD) The molecular mechanism of anti-dementia medicine. Methods: Sixty Kunming mice were randomly divided into six groups: blank control, model, Pirathiracetam, Naurikang, medium and low dose groups. Except the blank group, the other groups were treated with aluminum chloride (AlCl3) 100 mg.kg-1 ip was given to the rats in the blank group, and the rats in the blank group were given the same amount of saline ip. All the rats were administered Naolerkan (34, 17, 8.5 g.kg-1.d-1) Pirazacan group was treated with pyrazinamide (10 gL-1) ig, and the blank group and model group were given the same amount of normal saline ig. The learning and memory scores of AD model mice were detected by jumping platform method. The expression of APP and Aβ in cerebral cortex and hippocampus of AD model mice was observed by immunohistochemical staining. The APP and Aβpositive substances were detected by image signal acquisition Gradient analysis with the analysis system. Results: Compared with the control group, the latent period of learning and memory in the model group was significantly shorter (P <0.01), the learning latency was significantly longer (P <0.05) and the number of errors in learning and memory was significantly increased (P <0.01) The memory latency was significantly longer (P <0.01), learning latency was significantly shorter (P <0.05), learning and memory errors were significantly reduced (P <0.01). The expressions of APP and Aβ in the brain of each model group were decreased to different extents (P <0.05 or P <0.01). There was a significant dose-effect relationship between the three dosage groups. Conclusion: Er’er-kang has significant anti-dementia effect on AD model of chronic aluminum poisoning. Its mechanism may be related to the regulation of APP and Aβ expression.