Objective:To observe the effect of acupuncture on the expression of mitochondrial proteome in hippocampus of senescence-accelerated mouse prone g (SAMPg) mice models with Alzheimer disease (AD),and to explore the possible protective mechanism of acupuncture on mitochondria.Methods:Sixty 6-month-old male SAMP8 mice were randomly divided into an acupuncture at acupoint group,an acupuncture at non-acupoint group and a model group,20 mice in each group.The 20 male senescence-accelerated mouse/resistance 1 (SAMR1) mice of the same age were used as a normal control group.Shenshu (BL 23),Baihui (GV 20),Xuehai (SP 10) and Geshu (BL 17) were selected for acupuncture intervention in acupuncture at acupoint group.After an 8-week intervention,mitochondrial tissues were extracted from the hippocampus.Differentially expressed proteins were identified by subcellular organelle proteomics.Western blot was used to verify the expressions of some related proteins in hippocampal mitochondria.Results:Compared with the model group,there were 13 differentially expressed protein spots in the acupuncture at acupoint group,of which,9 were up-regulated,including neurofilament light polypeptide (NFL),actin (cytoplasmic 1,database ID:ACTB),tubulin beta-2A chain (TBB2A),tropomodulin-2 (TMOD2),pyruvate dehydrogenase E1 component subunit beta (PDHE1-β),NADH-ubiquinone oxidoreductase 75 kDa subunit (database ID:NDUS1),heat shock cognate 71 kDa protein (HSC71),pyruvate dehydrogenase E1 component subunit alpha (PDHE1-α) and ATP synthase beta subunit (ATP-β);4 were down-regulated,including glial fibrillary acidic protein (GFAP),pyruvate dehydrogenase phosphatase 1 (PDP1),mitochondrial-processing peptidase subunit alpha (MMP-α) and adenosine kinase (ADK).According to the information provided in the protein database,most of the differentially expressed proteins involve the regulation of mitochondrial function and structure.The expression levels of NFL and TBB2A in the normal control group and the acupuncture at acupoint group were significantly higher than those in the acupuncture at non-acupoint group (P＜0.05).ATP-β and NDUS1 expression levels were significantly higher in the acupuncture at acupoint group than those in the acupuncture at non-acupoint group (P＜0.05);there was no significant difference between the acupuncture at non-acupoint group and the model group (P＞0.05).Conclusion:Acupuncture may achieve the potential therapeutic effect on AD by regulating the structure and functional proteins of hippocampal mitochondria.

Objective To investigate the effects of Bushen Huoxue acupuncture method on the behavioral changes and the proliferation of endogenous neural stem cells (NSCs) in hippocampus of Alzheimer disease (AD) model mice. Methods 18 male SAMP8 mice, seven months old, were randomly divided into acupuncture group, non-acupoint control group, and model control group. And another age-matched 6 male SAMR1 mice were prepared as normal control group. Mice in acupuncture group were intervened by acupuncture method in the acupoints of "Shenshu", "Baihui", "Xuehai", and "Geshu". Mice in non-acupoint control group were treated by stimulating the fixed non-point under the bilateral rib, while mice in model control group and normal control group were raised without special treatment but administered the stimulation of catching with the same time and the same stimulus intensity. All treatrment lasted for 8 weeks. After the intervention, the learning and memory abilitities and brain hippocampus Brd U positive cells of all groups were detected. Results Compared with the nomal control group, mice in the model control group had longer escape latency and less time spent in former platform quadrant (P＜0.05); the number of Brd U positive cells decreased significantly (P＜0.05). Compared with the model control group and the non-acupoint control group, mice in the acupuncture group had shorter escape latency and more time spent in former platform quadrant (P＜0.05); the number of Brd U positive cells increased significantly (P＜0.05). Conclusion Bushen Huoxue acupuncture method can improve the learning and memory abilities of SAMP8 mice AD model by inducing the proliferation of hippocampal endogenous NSCs.