脑尔康对老年痴呆小鼠脑内胆碱酯酶活性及神经元的影响

Effect of compound traditional Chinese herb Nao Er Kang on acetylcholinesterase and neuron in model mice with alzheimer's disease

目的 通过慢性铝中毒造成老年痴呆小鼠模型。观察复方中药脑尔康对小鼠学习记忆障碍的保护作用 ,探讨其对胆碱酯酶活性的影响及保护神经元的抗痴呆作用机理。方法 健康昆明种雄性小鼠 60只 ,随机分为 6组 ,除空白组外 ,连续造模 50d后 ,每组随机取 3只 ,用HE染色法 ,观察小鼠海马CA1区细胞数量及形态 ,其余动物迅速断头取脑 ,冰台分离海马及皮层 ,检测各自的胆碱脂酶活性。结果 模型组AchE活性明显增高 (P <0 0 1 ) ,用药各组与模型组比较 ,除小剂量组外AchE活性均明显低于模型组 (P <0 0 1 ) ;模型组海马CA1区神经元数量明显少于空白组 (P <0 0 1 ) ,可见神经元脱失 ,并有胶质细胞增生。用药各组与模型组比较 ,只有中药大、中剂量组神经元数量显著多于模型组 (P <0 0 5或P <0 0 1 )。结论 脑尔康能明显降低老年痴呆模型小鼠皮层及海马AchE活性 ,保护海马CA1区神经元的作用。

Objective To observe the protective effect of compound traditional Chinese herb Nao Er Kang on learning and memorizing disorders in model mice with Alzheimers disease (AD) caused by aluminum chloride and to evaluate Nao Er Kang effect on activity of acetylcholinesterase and the mechanism of anti dementia by protecting neuron.Methods Sixty Kunming healthy mice were divided into 6 groups randomly.Fifty days later,three mice in each group were randomly and respectively selected.The morphological features of hippocampus cell were observed by HE (Hematoxylin and Eosin) staining and quantities of cell were recorded in CA1 region.The brains of other mice were got after decollated rapidly.After hippocampus and cortex were detached on ice table,the activity of their acetyl cholinesterase was determined separatedly. Results The activity of AchE was strengthened largely in model group.But compared with the model group,the activity of AchE was obviously lower ( P <0 01) in the medicated groups except the small dose group.The quantities of model group neuron were less than that of control group neuron ( P <0.01) in the CA1 region of hippocampus,and the loss of neuron and hyperplasia of colloid cells could be observed. Compared to the model group , the quantities of survived neuron in the medicated group were more ( P <0.05 or P <0.01) when large dose and normal dose Nao Er Kang were given separatedly.Conclusion Nao Er Kang can obviously suppress the activity of AchE in cortex and hippocampus,so as to protect CA1 region neuron in mice with AD.