电针对APP/PS1双转基因老年性痴呆模型小鼠认知能力及海马NMDARs表达的影响  

Effects of Electroacupuncture on Cognition and Expression of NMDARs in Hippocampus of Alzheimer.s Disease Mice

作　　者：许安萍[1] 王鑫 韩丽 李志刚[1] Xu Anping;Wang Xin;Han Li;Li Zhigang(School of Acupuncture-Moxibustion and Tuina,Beijing University of Chinese Medicine,Beijing 100029,China;Beijing Hospital of Traditional Chinese Medicine,Capital Medical University,Beijing,100010,China;School of Traditional Chinese,Beijing University of Chinese Medicine,Beijing 100029,China)

机构地区：[1]北京中医药大学针灸推拿学院,北京100029 [2]首都医科大学附属北京中医医院,北京100010 [3]北京中医药大学中医学院,北京100029

出　　处：《世界科学技术-中医药现代化》2020年第8期2652-2657,共6页Modernization of Traditional Chinese Medicine and Materia Medica-World Science and Technology

基　　金：国家自然科学基金委员会青年基金项目(81503654):逆针灸对老年性痴呆小鼠“抗衰老基因”KLOTHO的调控,负责人:许安萍;中央高校基本科研业务费专项资金资助基金项目(NO.2020-JYB-ZDGG-065):基于mTOR信号通路探讨针刺井穴防治阿尔茨海默病的机制研究,负责人:许安萍

摘　　要：目的研究电针是否通过调节老年性痴呆模型小鼠海马N-甲基-D-天冬氨酸型谷氨酸受体(NMDARs)的表达,保护认知能力,探讨电针防治老年性痴呆的作用机制。方法16只6月龄雄性APPswe/PS1 dE9(APP/PS1)双转基因小鼠作为老年性痴呆动物模型,采用随机数字表法分为痴呆模型组及电针治疗组,每组8只;以同月龄C57BL/6J野生型小鼠8只为对照组。选用百会穴、印堂穴及水沟穴,电针治疗20 min/次,隔日干预1次。治疗4周后,运用Morris水迷宫测试观察电针治疗对实验小鼠认知能力的影响,以Western Blot法检测小鼠海马NMDARs表达水平。结果痴呆模型组小鼠逃避潜伏期较对照组增加,第Ⅲ象限平台穿越次数及停留时间均减少;海马NMDAR1及NMDAR2B的蛋白表达水平下降。与痴呆模型组比较,电针治疗组逃避潜伏期明显减少;NMDAR1及NMDAR2B的表达增加。结论电针可改善老年性痴呆模型小鼠学习记忆能力,其机制可能与增加海马NMDARs表达有关。Objective To observe whether expression of NMDARs in hippocampus can be adjusted by electroacupuncture(EA)to enhance the cognition of Alzheimer’s disease(AD)mice,and to explore the mechanism of the EA therapy for AD.Methods Sixteen 6-month-old APPswe/PS1 dE9(APP/PS1)transgenic mice were randomly divided into AD model group and EA treatment group,eight in each group,with eight C57 BL/6 wild type mice as the normal control group.Baihui(GV20),Yintang(GV29)and Shuigou(GV26)were applied,EA treatment for 20 min every other day.After 4 weeks,Morris water maze test was used to evaluate the learning and memory ability of mice,and Western Blot was used to detect the expression level of NMDARs in the hippocampus of mice.Results The escape latency in the AD model group was significantly higher than that in the normal control group,while platform crossover number and the percentage of duration in the third quadrant of AD model group were significantly reduced;the expressions of NMDARI and NMDAR2 B in the hippocampus were significantly decreased.Compared with AD model group,the escape latency in EA treatment group was significantly decreased,the levels of NMDAR1 and NMDAR2 B in the hippocampus were significantly increased.Conclusion EA therapy can improve the cognition of the AD mice.The mechanism may be related to the increased expression of NMDARs in hippocampus.

关 键 词：老年性痴呆 电针 海马 认知能力 N-甲基-D-天冬氨酸型谷氨酸受体 

分 类 号：R245[医药卫生—针灸推拿学]