title: Electroacupuncture pretreatment induces tolerance against focal cerebral ischemia through activation of canonical Notch pathway.
abstract: BACKGROUND
  Electroacupuncture (EA) pretreatment can induce the tolerance against focal cerebral ischemia. However, the underlying mechanisms have not been fully understood. Emerging evidences suggest that canonical Notch signaling may be involved in ischemic brain injury. In the present study, we tested the hypothesis that EA pretreatment-induced tolerance against focal cerebral ischemia is mediated by Notch signaling.
  
  
  RESULTS
  EA pretreatment significantly enhanced Notch1, Notch4 and Jag1 gene transcriptions in the striatum, except Notch1 intracellular domain level, which could be increased evidently by ischemia. After ischemia and reperfusion, Hes1 mRNA and Notch1 intracellular domain level in ischemic striatum in EA pretreatment group were increased and reached the peak at 2 h and 24 h, respectively, which were both earlier than the peak achieved in control group. Intraventricular injection with the γ-secretase inhibitor MW167 attenuated the neuroprotective effect of EA pretreatment.
  
  
  CONCLUSIONS
  EA pretreatment induces the tolerance against focal cerebral ischemia through activation of canonical Notch pathway.
authors.affiliation: Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. houlihong@fmmu.edu.cn.
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhao
authors.forename: Xiyao
authors.initials: X
authors.lastname: Chen
authors.forename: Lei
authors.initials: L
authors.lastname: Ma
authors.forename: Zhiyi
authors.initials: Z
authors.lastname: Zuo
authors.forename: Zhenghua
authors.initials: Z
authors.lastname: Zhu
authors.forename: Xiaoling
authors.initials: X
authors.lastname: Zhu
authors.forename: Qiang
authors.initials: Q
authors.lastname: Wang
authors.forename: Ertao
authors.initials: E
authors.lastname: He
authors.forename: Lize
authors.initials: L
authors.lastname: Xiong
authors.forename: Jianming
authors.initials: J
authors.lastname: Pei
authors.forename: Lixian
authors.initials: L
authors.lastname: Xu
authors.forename: Lihong
authors.initials: L
authors.lastname: Hou
authors.forename: Shaoyang
authors.initials: S
authors.lastname: Chen
mesh_terms: D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins / Q000235:genetics / Q000378:metabolism; D020520:Brain Infarction / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D015671:Electroacupuncture; D004791:Enzyme Inhibitors / Q000009:adverse effects; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000188:drug therapy / Q000378:metabolism* / Q000517:prevention & control*; D008297:Male; D009422:Nervous System Diseases / Q000188:drug therapy / Q000209:etiology / Q000517:prevention & control; D010455:Peptides / Q000009:adverse effects; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D051880:Receptors, Notch / Q000235:genetics / Q000378:metabolism*; D015424:Reperfusion; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology* / Q000528:radiation effects; D013997:Time Factors; D000072056:Transcription Factor HES-1
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D004791:Enzyme Inhibitors; D018398:Homeodomain Proteins; D010455:Peptides; D012333:RNA, Messenger; D051880:Receptors, Notch; D000072056:Transcription Factor HES-1; C489735:Hes1 protein, rat; C432344:MW167