title: Involvement of ERK 1/2 activation in electroacupuncture pretreatment via cannabinoid CB1 receptor in rats.
abstract: Our previous study demonstrated that pretreatment with electroacupuncture (EA) elicited protective effects against transient cerebral ischemia through cannabinoid receptor type 1 receptor (CB1R). In the present study, we investigated whether or not the extracellular signal regulated-kinase 1/2 (ERK1/2) pathway was involved in the ischemic tolerance induced by EA pretreatment through CB1R. At 24h after the end of the last EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion for 120min in rats. The neurological scores and infarct volumes were evaluated at 24h after reperfusion. The expression of p-ERK1/2 in the brains was also investigated in the presence or absence of CB1R antagonist AM251. EA pretreatment reduced infarct volumes and improved neurological outcome at 24h after reperfusion, and the beneficial effects were abolished by U0126. The blockade of CB1R by AM251 reversed the up-regulation of p-ERK1/2 expression induced by EA pretreatment. Our findings suggest that the ERK1/2 pathway might be involved in EA pretreatment-induced cerebral ischemic tolerance via cannabinoid CB1 receptor in rats.
authors.affiliation: Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
authors.forename: Juan
authors.initials: J
authors.lastname: Du
authors.forename: Qiang
authors.initials: Q
authors.lastname: Wang
authors.forename: Bo
authors.initials: B
authors.lastname: Hu
authors.forename: Zhengwu
authors.initials: Z
authors.lastname: Peng
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhao
authors.forename: Lei
authors.initials: L
authors.lastname: Ma
authors.forename: Lize
authors.initials: L
authors.lastname: Xiong
authors.forename: Yan
authors.initials: Y
authors.lastname: Lu
authors.forename: Xiaoling
authors.initials: X
authors.lastname: Zhu
authors.forename: Shaoyang
authors.initials: S
authors.lastname: Chen
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D015153:Blotting, Western; D002545:Brain Ischemia / Q000503:physiopathology / Q000523:psychology; D002070:Butadienes / Q000494:pharmacology; D015671:Electroacupuncture; D004789:Enzyme Activation / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D020244:Infarction, Middle Cerebral Artery / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000473:pathology / Q000523:psychology; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000494:pharmacology; D009570:Nitriles / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D011720:Pyrazoles / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D043884:Receptor, Cannabinoid, CB1 / Q000502:physiology*; D015427:Reperfusion Injury / Q000473:pathology; D015398:Signal Transduction / Q000502:physiology; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D002070:Butadienes; D004791:Enzyme Inhibitors; D018696:Neuroprotective Agents; D009570:Nitriles; D010880:Piperidines; D011720:Pyrazoles; D043884:Receptor, Cannabinoid, CB1; C113580:U 0126; C103505:AM 251; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3