[Effect of electroacupuncture on complement C1q and microglia phagocytosis in hippocampus of SAMP8 mice].

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 (P<0.01), duration of swimming in the original platform quadrant and the number of original platform crossing were significantly shorter and decreased respectively (P<0.01). Compared with the model group, the average escape latency in the EA group was shortened (P<0.05, P<0.01), the duration of swimming in the original platform quadrant and the number of original platform crossing were significantly prolonged and increased (P<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 (P<0.01, P<0.05), and obviously down-regulated except the mRNA expression level of hippocampal Iba-1 in the EA group relevant to the model group (P<0.01, P<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.目的：观察电针对SAMP8小鼠海马区离子钙结合衔接分子1(Iba-1)、补体C1q、分化簇68(CD68)表达水平的影响，探讨电针治疗阿尔茨海默病的作用机制。方法：SAMP8小鼠随机分为模型组与电针组，每组12只，并以12只同月龄SAMR1小鼠作为对照组。电针组予“百会”“大椎”“肾俞”电针治疗，20 min/次，1次/d，8 d为1个疗程，共干预3个疗程，疗程之间间隔2 d。采用Morris水迷宫实验观察小鼠学习记忆能力，免疫组织化学法检测海马CA1区Iba-1、CD68蛋白阳性表达水平，Western blot法和实时荧光定量PCR法检测海马组织Iba-1、C1q、CD68蛋白和mRNA的表达水平。结果：与对照组比较，模型组平均逃避潜伏期延长(P<0.01)，原平台象限停留时间缩短、跨越原平台的次数减少(P<0.01)；与模型组比较，电针组平均逃避潜伏期缩短(P<0.05，P<0.01)，原平台象限停留时间延长、跨越原平台次数增加(P<0.01)。与对照组比较，模型组海马CA1区Iba-1、CD68蛋白阳性表达及海马组织Iba-1、C1q、CD68蛋白和mRNA表达水平升高(P<0.01，P<0.05)；与模型组比较，电针组海马CA1区Iba-1、CD68蛋白阳性表达及海马组织Iba-1蛋白及C1q、CD68蛋白和mRNA表达水平降低(P<0.01，P<0.05)。结论：电针能改善SAMP8小鼠学习记忆能力，其机制可能与抑制补体C1q依赖的小胶质细胞吞噬能力有关。.