[Protective function of electroacupuncture on young mouse model of Alzheimer's disease and proteomic study].

Objective: To screen protein target in prevention and treatment with electroacupuncture (EA) for Alzheimer's disease (AD) and explore the potential mechanism of EA in prevention of AD.
Methods: A total of 40 APP/PS1 transgenic young male mice, 1.5-month old, were randomized into an EA group and a model group, 20 mice in each one, and 20 C57BL/6J mice were chosen as the normal control group. After adaptive housing for 1 week, the mice in the EA group were stimulated with EA at "Baihui" (GV 20), "Fengfu" (GV 16) and "Shenshu" (BL 23), with intermittent wave, 10 Hz in frequency and 2 mA in electric intensity. EA was given once daily, 20 min each time. There was 1 day at interval after EA for 6 days each week. Totally, the intervention lasted for 16 weeks. On day 3 after the end of EA intervention, Morris water maze test was adopted to detect learning and memory abilities of mice in each group. After water maze test, the label-free method was used to measure the difference expressions in cerebral cortex and hippocampus. Using Western blot method, the expressions of guanylate binding protein beta 5 (GNB 5) and histone-H 3 in cerebral cortex and hippocampus were verified. Using immunohistochemical method, the expressions of amyloid beta protein (Aβ) in cerebral cortex and hippocampus were detected.
Results: Compared with the normal control group, the escape latency (on day 2, 3 and 4) was prolonged, the frequency of crossing platform and the duration of platform stay were decreased in the mice of the model group ( P <0.05). Compared with the model group, the escape latency (on day 3 and 4) was shortened, the frequency of crossing platform and the duration of platform stay were increased in the mice of the EA group ( P <0.05). By the comparison among the three groups, the high mobility group nucleosome-binding domain-containing protein 5, band 3 anion transport protein, histone-H 3, epoxide hydrolase 4 (fragment), neurolysin (mitochondria), phosphoglycerate mutase 2, GNB5 and Aβ were the differential proteins with the larger fold-change difference in expression. Compared with the normal control group, the expression of histone-H 3 in cerebral cortex and hippocampus was reduced ( P <0.001) and the expressions of GNB 5 and Aβ were increased ( P <0.001, P <0.01) in the mice of the model group. Compared with the model group, the expression of histone-H 3 in cerebral cortex and hippocampus was increased ( P <0.001) and the expressions of GNB 5 and Aβwere reduced ( P <0.001, P <0.05) in the mice of the EA group.
Conclusion: The intervention with EA effectively prevents from the decline of learning and memory ability and the formation of Aβ senile plaques in cerebral cortex and hippocampus in young mouse models of AD after growing up. Besides, EA plays a regulatory function for protein expression differences induced by AD model.