观察电针百会（GV20）和肾俞（BL23）对SAMP8小鼠神经病理损伤和神经修复的抗炎作用，为电针预防和治疗阿尔茨海默病提供新的实验依据。将12只7个月龄的SAMP8小鼠随机分为模型组和电针组，并使用相同年龄和遗传背景的6只SAMR1小鼠作为正常组。电针组小鼠在GV20和双侧BL23处接受针刺，并对双侧BL23施加EA（1 mA，2 Hz），每天1次，连续10天为1个疗程，共4个疗程，间隔1天。正常组和模型组小鼠的捕获和固定方式与电针组相同。利用Morris水迷宫测试检测空间学习和记忆能力。采用免疫荧光染色检测神经核抗原（NeuN）阳性表达和DG中NeuN阳性细胞数量。通过Western blot检测海马区离子钙结合适配分子1（Iba-1）、肿瘤坏死因子α（TNF-α）、白细胞介素（IL）-6和IL-1β蛋白表达水平。利用透射电子显微镜观察DG中的神经细胞超微结构。与正常组相比，模型组的平均逃脱潜伏期延长（P <0.01），平台穿越次数显着减少（P <0.01），海马体DG区的NeuN平均荧光强度和NeuN阳性细胞数量较少（P <0.05），海马区的Iba-1、TNF-α、IL-6和IL-1β表达水平增加（P <0.05）。与模型组相比，电针组的平均逃脱潜伏期缩短（P <0.01），平台穿越次数显着增加（P <0.01），海马体DG区的平均NeuN荧光强度和NeuN阳性细胞数量增加（P <0.05），海马区的Iba-1、TNF-α、IL-6和IL-1β表达水平降低（P <0.05）。正常组海马DG区神经细胞形态正常，细胞质中的细胞器清晰、完整且排列有序。而模型组的神经细胞形态严重不规则，在电针组中也不规则，但相对于模型组有所缓解。GV20和BL23处的电针可以提高SAMP8小鼠的学习和记忆能力，这可能与抑制神经炎症反应、增加神经元数量和改善海马体DG区超微结构以发挥神经保护作用有关。

To observe the effect of electroacupuncture (EA) at "Baihui"(GV20) and "Shenshu" (BL23) on the pathological injury of neurons in SAMP8 mice and the anti-inflammatory effect on neuron repair, providing a new experimental basis for EA prevention and treatment of Alzheimer's disease.Twelve 7-month-old SAMP8 mice were randomly divided into model and EA groups, and 6 SAMR1 mice of the same age and genetic background were used as normal group. Mice in the EA group were needled at GV20 and bilateral BL23, and EA (1 mA, 2 Hz) was applied to bilateral BL23 for 15 min, once daily, 10 d as a course for a total of 4 courses, with an interval of 1 d. Mice in the normal and model groups were captured and fixed in the same way as the EA group. The spatial learning and memory ability was detected by Morris water maze test. Neuronal nuclear antigen (NeuN) positive expression and the number of NeuN-positive cells in dentate gyrus (DG) were detected by immunofluorescence staining. The protein expression levels of ionized calcium binding adapter molecule 1(Iba-1), tumor necrosis factor-α(TNF-α), interleukin (IL)-6 and IL-1β in hippocampus were detected by Western blot. The ultrastructure of nerve cells in DG was observed by transmission electron microscopy.Compared with the normal group, the average escape latency was prolonged(P<0.01), the number of platform crossing was significantly reduced (P<0.01), the average fluorescence intensity of NeuN and the number of NeuN-positive cells in hippocampus DG region decreased (P<0.05), the expression levels of Iba-1, TNF-α, IL-6 and IL-1β in hippocampus were increased (P<0.05) in the model group.Compared with the model group, the ave-rage escape latency was shortened (P<0.01), the number of platform crossing times was significantly increased (P<0.01), the average fluorescence intensity of NeuN and the number of NeuN-positive cells in hippocampus DG region increased (P<0.05), the expression levels of Iba-1, TNF-α, IL-6 and IL-1β in hippocampus were decreased (P<0.05) in the EA group. The morphology of nerve cells in the hippocampus DG region was normal， and the organelles in the cytoplasm were clear, complete and regularly distributed in the normal group. However, the morphology of nerve cells in the model group was seriously irregular, which was also irregular in EA group but somewhat relieved compared with model group.EA at GV20 and BL23 can improve the learning and memory ability of SAMP8 mice, which may be related to inhibiting the neuroinflammatory response, increasing the number of neurons and improving the ultrastructure of the DG region of the hippocampus to play the role of neuron protection.