title: Electroacupuncture pretreatment induces tolerance against cerebral ischemia/reperfusion injury through inhibition of the autophagy pathway.
abstract: Electroacupuncture (EA) pretreatment has been reported to induce tolerance against cerebral ischemia/reperfusion (I/R) injury; however, the mechanisms underlying the beneficial effects of EA remain to be elucidated. Increasing evidence has suggested that excess activation of autophagy is important in I/R injury. The present study aimed to investigate the hypothesis that EA pretreatment‑induced tolerance to cerebral I/R injury was mediated by inhibition of the autophagy pathway. Rats were treated with EA at the acupoint 'Baihui (GV20)' 30 min/day, for five consecutive days prior to the induction of focal cerebral ischemia for 120 min by middle cerebral artery occlusion. Levels of autophagy, cerebral apoptosis, infarct volumes, brain water content and motor deficit were evaluated 12 h following I/R. The autophagy inducer rapamycin was used to investigate the role of autophagy in mediating neuroprotective effects. The results showed that the number of autophagosomes and the expression of the marker proteins of autophagy, including microtubule‑associated protein 1A light chain 3 (LC3)‑II and Beclin 1 were significantly increased 12 h post‑I/R. EA pretreatment decreased the expression of autophagy markers and the number of autophagosomes in the ischemic cortex. In addition, EA pretreatment inhibited neuronal apoptosis, reduced infarct volume and water content, as well as improved neurological outcome of rats following I/R. Furthermore, the reduced expression of LC3‑II and Beclin 1 and the neuroprotective effects were reversed by the autophagy inducer rapamycin. In conclusion, the results of the present study demonstrated that EA pretreatment protected the brain against I/R injury via inhibition of the autophagy process.
authors.affiliation: The First Clinical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China.
authors.forename: Zhouquan
authors.initials: Z
authors.lastname: Wu
authors.affiliation: Laboratory of Neurological Diseases, Department of Anesthesiology, Changzhou No. 2 People's Hospital, The Affiliated Hospital of Nanjing Medical University, Changzhou, Jiangsu 213003, P.R. China.
authors.forename: Zhiqing
authors.initials: Z
authors.lastname: Zou
authors.affiliation: The First Clinical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China.
authors.forename: Rong
authors.initials: R
authors.lastname: Zou
authors.affiliation: Department of Neurology, Changzhou No. 2 People's Hospital, The Affiliated Hospital of Nanjing Medical University, Changzhou, Jiangsu 213003, P.R. China.
authors.forename: Xianju
authors.initials: X
authors.lastname: Zhou
authors.affiliation: The First Clinical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China.
authors.forename: Suyang
authors.initials: S
authors.lastname: Cui
mesh_terms: D015669:Acupuncture Points; D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001343:Autophagy / Q000187:drug effects; D000071186:Beclin-1; D001921:Brain / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D015671:Electroacupuncture; D008297:Male; D046529:Microscopy, Electron, Transmission; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology*; D020123:Sirolimus / Q000633:toxicity
chemical_list: D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; D008869:Microtubule-Associated Proteins; D020123:Sirolimus; C512829:Becn1 protein, rat; C526109:Anxa3 protein, rat