Hong Miao-Miao, Zhao En-Cong, Chen Li-Min, Wang Feng, Guo Wan-Qing, Zheng Xue-Hua, Lin Lan, Li Chang-Zheng, Dong Wei-Guo
School of Acupuncture and Moxibustion, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
College of Integrated Chinese and Western Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Zhen Ci Yan Jiu. 2022 Jun 25;47(6):479-84. doi: 10.13702/j.1000-0607.20210573.
To observe the effect of electroacupuncture (EA) on the expression of Iba-1, complement C1q and CD68 in hippocampus of SAMP8 mice, so as to explore its mechanisms underlying improvement of Alzheimer's disease (AD).
Twenty-four male SAMP8 mice were randomly and equally divided into model and EA groups, and 12 SAMR1 mice were used as the control group. EA (2 Hz, 1.5-2.0 mA) was applied to "Baihui" (GV20), "Dazhui"(GV14) and "Shen-shu"(BL23) for 20 min once daily in the EA group, each course of treatment was 8 days, with an interval of 2 days between two courses, and the mice were treated for 3 courses. Morris water maze test was performed to assess the learning-memory ability of mice. The positive expression levels of Iba-1 and CD68 proteins in the hippocampus CA1 region were detected by immunohistochemistry. The mRNA and protein expression levels of Iba-1,C1q and CD68 in the hippocampus were detected by real-time PCR and Western blot, separately.
Compared with the control group, the average escape latency of Morris water maze test was prolonged in the model group (<0.01), duration of swimming in the original platform quadrant and the number of original platform crossing were significantly shorter and decreased respectively (<0.01). Compared with the model group, the average escape latency in the EA group was shortened (<0.05, <0.01), the duration of swimming in the original platform quadrant and the number of original platform crossing were significantly prolonged and increased (<0.01). The immunoactivity of Iba-1 and CD68 in hippocampal CA1 region, and mRNA and protein expression levels of hippocampal Iba-1,C1q and CD68 were significantly up-regulated in the model group in contrast to the control group (<0.01, <0.05), and obviously down-regulated except the mRNA expression level of hippocampal Iba-1 in the EA group relevant to the model group (<0.01, <0.05).
EA can improve the learning and memory ability of SAMP8 mice, which may be associated with its effect in inhibiting of complement C1q-dependent microglial phagocytosis in the hippocampus.
观察电针（EA）对快速老化模型小鼠（SAMP8）海马中离子钙结合衔接分子1（Iba-1）、补体C1q和CD68表达的影响，以探讨其改善阿尔茨海默病（AD）的机制。
将24只雄性SAMP8小鼠随机等分为模型组和电针组，另取12只SAMR1小鼠作为对照组。电针组给予“百会”（GV20）、“大椎”（GV14）和“肾俞”（BL23）电针治疗（2Hz，1.5 - 2.0mA），每次20分钟，每日1次，每个疗程8天，疗程间隔2天，共治疗3个疗程。采用Morris水迷宫试验评估小鼠学习记忆能力。免疫组化法检测海马CA1区Iba-1和CD68蛋白的阳性表达水平。分别采用实时荧光定量PCR和蛋白质免疫印迹法检测海马中Iba-1、C1q和CD68的mRNA和蛋白表达水平。
与对照组相比，模型组Morris水迷宫试验平均逃避潜伏期延长（<0.01），在原平台象限游泳时间和穿越原平台次数明显缩短和减少（<0.01）。与模型组相比，电针组平均逃避潜伏期缩短（<0.05，<0.01），在原平台象限游泳时间和穿越原平台次数明显延长和增加（<0.01）。与对照组相比，模型组海马CA1区Iba-1和CD68免疫活性及海马Iba-1、C1q和CD68的mRNA和蛋白表达水平显著上调（<0.01，<0.05）；与模型组相比，电针组除海马Iba-1的mRNA表达水平外，其余均明显下调（<0.01，<0.05）。
电针可改善SAMP8小鼠的学习记忆能力，其机制可能与抑制海马中补体C1q依赖的小胶质细胞吞噬作用有关。
