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目的建立铝致老年痴呆症(AD)小鼠模型,探讨中药干预效果及机制。方法小鼠给予氯化铝水溶液拌饲料喂养建立AD模型,实验设对照组、模型组、抗痴1、2、3号组(n=6)。采用水迷宫试验测定小鼠记忆力变化,处死小鼠取大脑,分别测定乙酰胆碱酯酶(AchE)、丙二醛(MDA)、铝含量、超氧阴离子自由基(O2·-)清除率,观察大脑病理改变。结果水迷宫实验结果显示,与对照组比较,模型组小鼠错误率明显升高;与模型组比较,抗痴1、2号组小鼠错误率明显下降(P<0.05);对照组、模型组、抗痴1、2、3号组AchE活性分别为(0.829±0.095)、(0.399±0.093)、(0.758±0.025)、(0.700±0.086)、(0.418±0.066)U/mg·prot,与对照组比较,模型组小鼠脑组织AchE活性下降,与模型组比较,抗痴1、2组小鼠脑组织AchE活性升高(P<0.01);与对照组比较,模型组小鼠脑组织O2·-清除率[(16.61±1.49)%]下降,与模型组比较,抗痴1、2号组小鼠脑组织O2·-清除率[分别为(20.54±1.93)%、(19.62±1.63)%]明显升高(P<0.05);模型组小鼠脑组织铝含量明显高于对照组,与模型组比较,抗痴干预各组小鼠脑组织中铝含量明显下降,差异有统计学意义(P<0.05);病理观察可见模型组小鼠脑神经细胞减少、神经元变性等损伤现象,抗痴干预组脑组织病理改变较轻。结论铝可致小鼠记忆认知能力障碍,大脑乙酰胆碱酯酶活性下降、抗氧化能力降低,中药可明显改善铝致小鼠神经毒性作用。
Objective To establish a mouse model of Alzheimer’s disease (Alzheimer’s disease) caused by aluminum and to explore the effect and mechanism of traditional Chinese medicine intervention. Methods The mice were fed with aluminum chloride aqueous solution to establish AD model. The control group, model group and anti-crazy 1,2,3 group (n = 6) were set up. The water maze test was used to measure the change of memory in mice. The mice were sacrificed and the brain was sacrificed. The clearance rate of acetylcholinesterase (AchE), malondialdehyde (MDA), aluminum, and superoxide anion free radicals (O2 · - Pathological changes. Results The results of water maze test showed that compared with the control group, the error rate of mice in the model group was significantly increased. Compared with the model group, the error rate of mice in the anti-crazy group 1,2 was significantly decreased (P <0.05) The activities of AchE in group 1 and group 2 were (0.829 ± 0.095), (0.399 ± 0.093), (0.758 ± 0.025), (0.700 ± 0.086) and (0.418 ± 0.066) U / mg · prot, Compared with the control group, the AchE activity in the brain tissue of mice in the model group decreased. Compared with the model group, the AchE activity in the brain tissue of the mice in the anti-crazy group 1 and 2 increased (P <0.01). Compared with the control group, Compared with the model group, the O2 · - clearance rate of brain tissue in anti-crazy 1,2 group were (20.54 ± 1.93)% and (19.62 ± 1.63)%] significantly increased (P <0.05). The content of aluminum in model group was significantly higher than that in control group. Compared with model group, the content of aluminum in brain of mice in each group decreased obviously (P <0.05). Pathological observation showed that in the model group, the damage of neurons and degeneration of neurons in the model group was lessened, and the pathological changes in the brain tissue of the anti-crazy group were lighter. Conclusion Aluminum can cause cognitive impairment of memory in mice, decline of acetylcholinesterase activity in the brain and decrease of anti-oxidation ability. Alzheimer’s disease can significantly improve the neurotoxicity induced by aluminum in mice.