title: Electroacupuncture promotes neurological functional recovery via the             retinoic acid signaling pathway in rats following cerebral ischemia-reperfusion             injury.
abstract: Neurogenesis is regulated by a number of signaling pathways, including the             retinoic acid (RA) pathway, a key regulator of neurogenesis in the subventricular             zone (SVZ) and hippocampus. Acupuncture has been used to treat neurological conditions             and is known to potentially enhance cell proliferation in the neurogenic area             (hippocampal dentate gyrus and the SVZ of the lateral ventricle walls) in pathological             conditions, which is associated with improved brain function. However, whether             or not the neuroprotective effects of electroacupuncture (EA) are mediated by             the regulation of the RA signaling pathway remains to be determined. Using a transient             middle cerebral artery occlusion model, in the present study we evaluated the             effect of EA on the neurological functional recovery, infarction volume and investigated             the underlying molecular mechanisms. Two hundred and sixteen SD rats were randomly             divided into 3 groups: sham, model group (ischemic rats without EA stimulation)             and EA group (ischemic rats with EA stimulation on ST36 and LI11). Behavioral             deficits were detected with high-resolution digital analysis of 24-h home-cage             video recordings. Infarct volume was determined by triphenyltetrazolium hydrochloride             staining and the expression of RA mRNA and protein was measured using RT-PCR and             western blotting, respectively. We found that EA decreased the infarct volume,             promoted neurological functional recovery and increased the RA mRNA and protein             expression, compared with the model group. Findings of this study suggest that             promoting neurological functional recovery by modulating RA expression in the             post-ischemic brain is one of the mechanisms by which EA can be effective in the             treatment of ischemic stroke.
authors.affiliation: Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, PR China.
authors.forename: Jiangcong
authors.initials: J
authors.lastname: Hong
authors.forename: Guangwen
authors.initials: G
authors.lastname: Wu
authors.forename: Yulong
authors.initials: Y
authors.lastname: Zou
authors.forename: Jing
authors.initials: J
authors.lastname: Tao
authors.forename: Lidian
authors.initials: L
authors.lastname: Chen
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000473:pathology / Q000628:therapy; D049109:Cell Proliferation / Q000187:drug effects; D004195:Disease Models, Animal; D015671:Electroacupuncture; D006624:Hippocampus / Q000503:physiopathology; D020244:Infarction, Middle Cerebral Artery / Q000473:pathology / Q000628:therapy; D020547:Lateral Ventricles / Q000503:physiopathology; D008297:Male; D055495:Neurogenesis / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D015427:Reperfusion Injury / Q000628:therapy*; D015398:Signal Transduction; D020521:Stroke / Q000473:pathology / Q000628:therapy; D013778:Tetrazolium Salts / Q000378:metabolism; D014212:Tretinoin / Q000378:metabolism*
chemical_list: D013778:Tetrazolium Salts; D014212:Tretinoin; C009591:triphenyltetrazolium