[Effect of electroacupuncture stimulation of "Baihui" (GV 20) and " Yongquan" (KI 1) on expression of hippocampal amyloid-β and low density lipoprotein receptor-related protein-1 in APP/PS 1 transgenic mice].
[Effect of electroacupuncture stimulation of "Baihui" (GV 20) and " Yongquan" (KI 1) on expression of hippocampal amyloid-β and low density lipoprotein receptor-related protein-1 in APP/PS 1 transgenic mice].
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发表时间：
2015-02
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通讯作者：
Fu Li;Li-na Li-Li-na-Li-49192469;Xin Wang;Yang Bai;Abulizi Jiawula;Qing-yun Bu;Tang-ke Gao;Weiguo Xue
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作者：
Fu Li;Li-na Li-Li-na-Li-49192469;Xin Wang;Yang Bai;Abulizi Jiawula;Qing-yun Bu;Tang-ke Gao;Weiguo Xue
目的观察电针对APP/PS 1转基因小鼠海马淀粉样β肽（Aβ）及其关键转运受体低密度脂蛋白受体相关蛋白1（LRP 1）水平的影响，探讨电针改善阿尔茨海默病（AD）的作用机制。方法将24只雄性APP/PS 1转基因小鼠随机分为模型组和电针治疗组，每组14只，另取12只C57 BL/6小鼠作为正常对照组。电针（1Hz/50 Hz，0.3mA）“百会”、“涌泉”穴15 min，隔日1次，共6周。采用Morris水迷宫实验检测大鼠学习记忆能力，ELISA法检测左侧海马Aβ 1-40和Aβ 1-42含量，Western blot法检测右侧海马LRP 1表达。结果Morris水迷宫实验结果显示，三组大鼠在逃避潜伏期、平台-位置交叉次数、在目标平台象限停留时间方面差异无统计学意义（P>0.05）。与模型组比较，电针治疗组大鼠中度增高的逃避潜伏期有降低趋势。ELISA检测结果显示，模型组大鼠海马Aβ 1-42、Aβ 1-40及Aβ 1-42/Aβ 1-40比值均显著高于正常对照组（P0. 05）。结论电针干预可降低APP/PS 1转基因小鼠海马Aβ水平，但对Aβ转运受体LRP 1表达及学习记忆能力的影响有待进一步证实。
OBJECTIVE 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). METHODS 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 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 (P0.05). CONCLUSION 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.