Objective 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). Methods 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. Results 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). Conclusion 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.