title: Electroacupuncture exerts anti-inflammatory effects in cerebral ischemia-reperfusion             injured rats via suppression of the TLR4/NF-κB pathway.
abstract: Inflammatory response has been shown to play a critical role in brain damage             after cerebral ischemia-reperfusion (I/R) injury, which is tightly regulated by             the Toll-like receptor (TLR)4/nuclear factor (NF)-κB pathway; therefore, suppression             of TLR4/NF-κB signaling has become a promising target for the anti-inflammatory             treatment in ischemic stroke. Acupuncture has been used as a complementary and             alternative therapy practice that supplements conventional medicine. Numerous             studies have demonstrated the clinical efficacy of acupuncture in stroke rehabilitation.             However, the precise mechanism of its neuroprotective effect remains poorly understood.             Using a focal cerebral I/R injured rat model, in the present study we evaluated             the neuroprotective and anti-inflammatory activities of electroacupuncture at             Quchi and Zusanli, and investigated the underlying molecular mechanisms. We found             that electroacupuncture at Quchi (LI11) and Zusanli (ST36) acupoints significantly             improved the ischemia-associated scores of neurological deficits, reduced cerebral             infarction and alleviated inflammatory responses. Moreover, the crucial signaling             molecules in the TLR4/NF-κB signaling pathway were regulated by acupuncture, which             coincided with suppressed secretion levels of inflammatory cytokines such as TNF-α,             IL-1β and IL-6. Our data suggest that electroacupuncture exerts a neuroprotective             function in ischemic stroke through inhibition of TLR4/NF-κB-mediated inflammation.
authors.affiliation: College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, PR China.
authors.forename: Lan
authors.initials: L
authors.lastname: Lan
authors.forename: Jing
authors.initials: J
authors.lastname: Tao
authors.forename: Azhen
authors.initials: A
authors.lastname: Chen
authors.forename: Guanli
authors.initials: G
authors.lastname: Xie
authors.forename: Jia
authors.initials: J
authors.lastname: Huang
authors.forename: Jiumao
authors.initials: J
authors.lastname: Lin
authors.forename: Jun
authors.initials: J
authors.lastname: Peng
authors.forename: Lidian
authors.initials: L
authors.lastname: Chen
mesh_terms: D000818:Animals; D002544:Cerebral Infarction / Q000628:therapy*; D004195:Disease Models, Animal; D015671:Electroacupuncture / Q000379:methods*; D007249:Inflammation / Q000628:therapy*; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D016328:NF-kappa B; C495347:Tlr4 protein, rat; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha