title: [Electroacupuncture Intervention Inhibits the Decline of Learning-memory Ability and Overex- pression of Cleaved Caspase-3 and Bax in Hippocampus Induced by Isoflurane in APPswe/PS 1].
abstract: OBJECTIVE
  To investigate the protection mechanism of electroacupuncture (EA) therapy against Alzheimer's disease (AD)-like neurotoxicity induced by Isoflurane.
  
  
  METHODS
  Twenty-four APPswe/PS 1 dE9 double transgenic mice (one of the most extensively used transgenic mouse model of AD) and 24 littermate wild-type mice were randomly assigned into control (Con) group, isoflurane (Iso) group and EA group, respectively (n = 8 in each group). EA (2 Hz/100 Hz, 1 mA) was applied to "Baihui" (GV 20) and "Yongquan" (KI 1) for 15 min, once a day for 3 days. The transgenic mice were exposed to a closed box filled with 1.2% isoflurane + 30% O2 +70% N2 for 4 h. The animals' learning-memory ability was detected by Morris water maze test. The expression of cleaved Caspase-3 in the CA 1 area of hippocampus was detected by immunohistochemistry, and that of hippocampal Bcl-2 and Bax proteins detected by Western blot.
  
  
  RESULTS
  Compared with the wilde-type mice, the average escape latency of place navigation test was significantly longer, while the percentage of target-quadrant stay time and the target- platform crossing times of spacial probe test were marked decreased in AD + lso mice (P < 0.05). After acupuncture intervention, the abovementioned changes were reversed (P < 0.05). Correspondingly, compared with the AD-Con group, the number of hippocampal activated Caspase-3-positive cells and the expression of Bax protein were significantly increased in the AD-Iso group (P < 0.05). After EA intervention, the increased Caspase-3-positive cell number and Bax protein expression were remarkably down-regulated in the AD-EA group, and the decreased ratio of Bcl-2/Bax in AD-Iso mice was obviously up-regulated in AD-EA mice (P < 0.05). No significant changes were found in the average escape latency, the percentage of target-quadrant stay time and the target-platofrm corssing times, and inthe number of hippocampal activated Caspase-3-positive cells, the expression levels of hippocampal Bcl-2 and Sax and the ratio of Bcl-2/Bax in the three groups of wilde-type mice (P > 0.05).
  
  
  CONCLUSIONS
  EA intervention can improve the learning-memory ability in AD + Isoflurane mice, suggesting a reduction of AD-like neurotoxicity, which may be associated with its actions in inhibiting the overexpression of activated Caspase-3 and Bax proteins in the hippocampus.
authors.forename: Xiang-yu
authors.initials: XY
authors.lastname: Li
authors.forename: Le
authors.initials: L
authors.lastname: Xu
authors.forename: Chui-liang
authors.initials: CL
authors.lastname: Liu
authors.forename: Li-sha
authors.initials: LS
authors.lastname: Huang
authors.forename: Xiao-ying
authors.initials: XY
authors.lastname: Zhu
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism / Q000523:psychology* / Q000628:therapy*; D000818:Animals; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D015671:Electroacupuncture; D005260:Female; D006624:Hippocampus / Q000378:metabolism*; D006801:Humans; D007530:Isoflurane / Q000009:adverse effects*; D007858:Learning; D008568:Memory; D051379:Mice; D008822:Mice, Transgenic; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism*
chemical_list: D051028:bcl-2-Associated X Protein; D007530:Isoflurane; D053148:Caspase 3