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目的：研究电针对于SAMP8 模型小鼠海马区早老蛋白1(presenilian 1,PS1)表达的影响，探讨电针治疗阿尔兹海默病（AD）的作用机制。方法：将20 只SAMP8 小鼠（早老化小鼠）随机分为模型对照组、电针治疗组，每组10 只；10 只SAMR1 小鼠（正常老化小鼠）组成正常对照组。正常对照组和模型对照组正常饲养15 天，在电针治疗组治疗时抓取束缚一次，不做任何治疗；电针治疗组每天治疗前抓取束缚之后再进行电针治疗，治疗穴位选取“百会”、“印堂”、“人中”三穴，频率2 Hz，电流强度以小鼠头部微颤为宜，留针20 min，每日1 次，共15 天。电针治疗结束后，通过Morris 水迷宫实验观察小鼠的行为学变化；通过免疫组化观察 SAMP8 小鼠海马区PS1 蛋白表达情况；通过Western blot方法检测各组海马区的PS1 蛋白表达水平。结果：行为学中Morris水迷宫检测显示：模型组与正常对照组比较逃避潜伏时增加，空间探索实验穿越平台次数和平台象限游泳时间明显减少（P<0.05，P<0. 01）；电针治疗组逃避潜伏时明显减少，空间探索实验穿越平台次数和平台象限游泳时间明显增加(P<0.05)；免疫组化观察各组海马区PS1蛋白表达，电针治疗组较模型组明显降低；Western blot 结果显示PS1 蛋白在海马区表达水平，模型组高于正常对照组 (P<0.01)，而电针治疗组低于模型组(P<0.01)。结论：电针可以改善小鼠的学习记忆能力，而且电针治疗组海马区PS1蛋白含量明显低于模型组，电针治疗可能参与减弱PS1 蛋白的表达，降低Abeta水平，对于AD 治疗有益。

英文摘要:

Objective:To research the efffect of Electro-acupuncture on the PS1 protein expression in the hippocampus of mice SAMP8, and discuss the mechanism of the EA treatment on AD.Methods:Twenty 8-month-old SAMP8 mice were randomly divided into model group and EA group, with ten SAMR1 mice as the normal control group. All the groups feed in normal environment. Model group and normal group should be caught and bounded once when the EA group is being treated. "Baihui", "Yintang", "Renzhong" were selected as the EA treat points for EA group 20 min a day for 15 days. The current frequency is 2 Hz and current strength is appropriate when the head of mice is quivering. The learning-memorize ability of mice was assessed by Morris water maze when the treatment finished. Immunohistochemistral method was used to observe the PS1 protein expression in the hippocampus of mice. The contents of PS1 protein in hippocampus was tested by Western Blotting.Results:The Morris water maze test showed the escape latency of model group increased, the number of platform-site crossover and the swimming duration in platform quadrant of model group were reduced compared with the control group（P<0.05，P<0.01）; the escape latency of EA group reduced, while the crossing time and dwell time in the target quadrant increased compared with the model group(P<0.05). The Immunohistochemistral result showed that the PS1 protein in the hippocampus of EA group obviously decreased compared with the model group（P<0.01）. The Western Blotting result showed the contents of PS1 protein in the model group were higher than that in the control group（P<0.01）, while the EA group could reduce its expression（P<0.01).Conclusion:EA therapy can improve the learning-memorize ability of the SAMP8 mice and decrease the protein contents of A-beta and PS1 in hippocampus. The EA treatment might be a promising method to AD patients.

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