Li Fu, Li Li-na, Wang Xin, Bai Yang, Jiawula Abulizi, Bu Qing-yun, Gao Tang-ke, Xue Wei-guo
Zhen Ci Yan Jiu. 2015 Feb;40(1):30-4, 55.
To observe the effect of electroacupuncture (EA) treatment on the level of hippocampal amyloid-beta peptide (Aβ) and its key transport receptor low density lipoprotein receptor-related protein-1 (LRP 1) in APP/PS 1 transgenic mice so as to explore its mechanism underlying improvement of Alzheimer's disease (AD).
Twenty-four male APP/PS 1 transgenic mice were equally and randomly divided into model group and EA treatment group, and 12 C 57 BL/6 mice were used as the normal control group. EA (1 Hz/50 Hz, 0.3 mA) was applied to "Baihui" (GV 20) and "Yongquan" (KI 1) for 15 min, once every other day for 6 weeks. The learning-memory ability was detected by using Morris water maze testing, left hippocampal Aβ 1-40 and Aβ 1-42 contents were assayed by ELISA, and right hippocampal LRP 1 expression was detected using Western blot (WB).
Results of Morris water maze test showed no significant differences among the three groups in the escape latency, the times of the platform-site crossovers, the time spent in the target platform quadrant (P>0.05). Compared with the model group, the moderately increased escape latency had a decreasing tendency in the EA treatment group. ELISA assaying showed that hippocampal Aβ 1-42, Aβ 1-40, and ratio of Aβ 1-42/Aβ 1-40 of the model group were significantly higher than those of the normal control group (P<0.01). After EA intervention, the increased Aβ 1-42 , Aβ 1-40, and ratio of Aβ 1-42/Aβ 1-40 were remarkably down-regulated in the EA treatment group (P<0.01). WB detection displayed that the right hippocampal LRP 1 expression level of the model group was markedly lower than that of the normal control group (P<0.05). After EA treatment, LRP 1 expression level was moderately up-regulated but without significant difference between the model and EA treatment groups (P>0.05).
EA intervention can lower the level of hippocampal Aβ in APP/PS 1 transgenic mice, but its effects on Aβ transport receptor LRP 1 expression and learning-memory ability need being confirmed further.
观察电针治疗对APP/PS1转基因小鼠海马β淀粉样蛋白（Aβ）水平及其关键转运受体低密度脂蛋白受体相关蛋白1（LRP1）的影响，以探讨其改善阿尔茨海默病（AD）的机制。
将24只雄性APP/PS1转基因小鼠平均随机分为模型组和电针治疗组，另取12只C57BL/6小鼠作为正常对照组。采用1Hz/50Hz、0.3mA的电针刺激“百会”（GV20）和“涌泉”（KI1）15分钟，隔日1次，共6周。采用Morris水迷宫试验检测学习记忆能力，用ELISA法检测左侧海马Aβ1-40和Aβ1-42含量，用蛋白质免疫印迹法（WB）检测右侧海马LRP1表达。
Morris水迷宫试验结果显示，三组小鼠的逃避潜伏期、穿越平台次数、在目标平台象限停留时间比较，差异均无统计学意义（P>0.05）。与模型组相比，电针治疗组小鼠的逃避潜伏期虽有升高趋势，但升高幅度较小。ELISA检测显示，模型组海马Aβ1-42、Aβ1-40及Aβ1-42/Aβ1-40比值均显著高于正常对照组（P<0.01）。电针干预后，电针治疗组升高的Aβ1-42、Aβ1-40及Aβ1-42/Aβ1-40比值均显著下调（P<0.01）。WB检测显示，模型组右侧海马LRP1表达水平显著低于正常对照组（P<0.05）。电针治疗后，LRP1表达水平有一定上调，但模型组与电针治疗组比较差异无统计学意义（P>0.05）。
电针干预可降低APP/PS1转基因小鼠海马Aβ水平，但其对Aβ转运受体LRP1表达及学习记忆能力的影响尚需进一步证实。
