目的:观察"通督启神"针法对老年痴呆模型小鼠空间学习记忆能力,大脑海马区神经元形态以及Aβ1-42蛋白、TREM2、DAP12的表达情况,探索"通督启神"电针法治疗老年性痴呆的作用机制。方法:将20只SAMP8小鼠随机分为老年痴呆组和"通督启神"电针组,10只同背景SAMR1小鼠作为正常对照组。"通督启神"电针组,穴取"百会"和"印堂"接电针,电针频率为2Hz,留针20min/d,并于电针治疗前点刺"人中"穴;正常对照组与老年痴呆组仅作束缚。治疗15d后,运用Morris水迷宫实验观察各组小鼠行为学变化;运用HE染色方法观察各组小鼠海马区神经元形态;运用免疫组化DAB染色法观察各组小鼠海马区Aβ1-42蛋白与TREM2、DAP12的表达情况;运用Western blot检测各组小鼠海马区TREM2、DAP12的表达含量。结果:"通督启神"针法可显著改善痴呆模型小鼠的空间学习记忆能力(P〈0.05,P〈0.01);可改善海马区神经元形态结构与Aβ1-42蛋白的表达情况(P〈0.01);并可促进TREM2与DAP12在海马区的表达(P〈0.05)。结论:"通督启神"针法可提高老年痴呆模型小鼠的空间学习记忆能力,改善海马区神经元形态结构与Aβ1-42蛋白的表达水平,其疗效作用的机制可能是通过提高海马区TREM2与DAP12的表达含量而发挥作用的。
Objective: To observe the influence of ‘Tongdu Qishen' acupuncture therapy on the spatial learning and memory ability, morphology neurons and expression of amyloid-β, TREM2 and DAP12 in hippocampal region of Alzheimer's disease(AD) model mice, and to explore the mechanism of ‘Tongdu Qishen' acupuncture therapy. Methods: Twenty SAMP8 mice were randomly divided into AD group and electro-acupuncture group, and 10 isomesic SAMR1 mice were as normal group. In electro-acupuncture group, Baihui(GV20) and Yintang(GV29) were treated by electro-acupuncture, frequency 2Hz for 20 min per day, and Shuigou(GV26) was treated by swift pricking blood therapy before the treatment of electro-acupuncture. Normal group and AD group were given constraint. After 15-day's treatment, morris water maze test was used to observe the ethology changes of mice in each group, HE staining method was used to observe the morphology of neurons in the hippocampal region of mice, immunohistochemical DAB staining was used to observe amyloid-β, TREM2 and DAP12 in hippocampal region of mice, Western blotting was used to observe TREM2 and DAP12 in hippocampal region of mice. Results: ‘Tongdu Qishen' acupuncture therapy could significantly improve the learning and memory ability of SAMP8 mice(P〈0.05, P〈0.01), inhibit the expression of amyloid-βin the hippocampus, and promote the expression of TREM2 and DAP12 in the hippocampus(P〈0.05). Conclusion: The ‘Tongdu Qishen' acupuncture therapy could improve the learning and memory ability of AD mice, improve the morphology of neurons in the hippocampal region, and inhibit the expression of amyloid-β in the hippocampus, its mechanism might be through increasing the expression levels of TREM2 and DAP12 in the hippocampal region.