Objective To observe the effect of electroacupuncture(EA) of “Xiusanzhen” [bilateral “Yingxiang”(LI20)+“Yintang”(GV24

+

)] on synaptophysin(SYN)

postsynaptic density protein-95(PSD-95)

Iba-1+)]

on synaptophysin(SYN)

postsynaptic density protein-95(PSD-95)

Iba-1

+

CD68+CD68

+

microglia and complement C related protein expression of hippocampus in Parkinson's disease dementia(PDD) mice

so as to explore its mechanism in improving memory impairment of PDD. Methods Male C57 BL/6 mice were randomly divided into control

sham operation

model and EA groups

with 10 mice in each group. The PDD model was established by injecting 6-OHDA into the medial forebrain tract. EA(2 Hz

1 mA) was applied to unilateral LI20 and GV29 for 20 min once daily for consecutive 14 days. Morris water maze and new object recognition test were used to evaluate the learning and memory ability. Western blot was used to detect the expression of SYN and PSD-95 proteins in hippocampus. Immunofluorescence was used to label Iba-1+ microglia and complement C related protein expression of hippocampus in Parkinson's disease dementia(PDD) mice

so as to explore its mechanism in improving memory impairment of PDD. Methods Male C57 BL/6 mice were randomly divided into control

sham operation

model and EA groups

with 10 mice in each group. The PDD model was established by injecting 6-OHDA into the medial forebrain tract. EA(2 Hz

1 mA) was applied to unilateral LI20 and GV29 for 20 min once daily for consecutive 14 days. Morris water maze and new object recognition test were used to evaluate the learning and memory ability. Western blot was used to detect the expression of SYN and PSD-95 proteins in hippocampus. Immunofluorescence was used to label Iba-1

+

CD68+CD68

+

microglia and C1 q positive cells in hippocampal CA1 region. The content of C3 protein in hippocampus was detected by ELISA. Results Compared with the control group

there was no statistical significance in all the observed indexes in the sham operation group. Compared with the sham operation group

the average escape latency(AEL) prolonged significantly(P

<

0.01)

the target platform crossing times(TPCT) and new object recognition index(NORI) decreased remarkably(P

<

0.01); the expressions of SYN and PSD-95 proteins in hippocampal CA1 region were significantly decreased(P

<

0.01); the rate of Iba-1+microglia and C1 q positive cells in hippocampal CA1 region. The content of C3 protein in hippocampus was detected by ELISA. Results Compared with the control group

there was no statistical significance in all the observed indexes in the sham operation group. Compared with the sham operation group

the average escape latency(AEL) prolonged significantly(P

<

0.01)

the target platform crossing times(TPCT) and new object recognition index(NORI) decreased remarkably(P

<

0.01); the expressions of SYN and PSD-95 proteins in hippocampal CA1 region were significantly decreased(P

<

0.01); the rate of Iba-1

+

CD68+CD68

+

microglia

the rate of C1 q positive cells and the content of C3 protein were significantly increased(P

<

0.01) in the model group. In comparison with the model group

the AEL was shortened(P

<

0.01)

the TPCT and NORI were increased(P

<

0.05) remarkably; the expressions of SYN and PSD-95 proteins in hippocampal CA1 region were increased(P

<

0.01

P

<

0.05); the rate of Iba-1+ microglia

the rate of C1 q positive cells and the content of C3 protein were significantly increased(P

<

0.01) in the model group. In comparison with the model group

the AEL was shortened(P

<

0.01)

the TPCT and NORI were increased(P

<

0.05) remarkably; the expressions of SYN and PSD-95 proteins in hippocampal CA1 region were increased(P

<

0.01

P

<

0.05); the rate of Iba-1

+

CD68+CD68

+

microglia

the rate of C1 q positive cells and the content of C3 protein were significantly decreased(P

<

0.01) in the EA group. Conclusion“Xiusanzhen” can alleviate the learning and memory impairment of PDD model mice

and improve the synaptic plasticity of hippocampal CA1 area. The mechanism may be related to the reduction of C1 q and C3 deposition in hippocampal CA1 region and the reduction of microglia phagocytosis.