title: Electroacupuncture ameliorates cognitive impairment through inhibition of NF-κB-mediated neuronal cell apoptosis in cerebral ischemia-reperfusion injured rats.
abstract: Cognitive impairment is a serious mental deficit following stroke that severely affects the quality of life of stroke survivors. Nuclear factor‑κB (NF-κB)-mediated neuronal cell apoptosis is involved in the development of post-stroke cognitive impairment; therefore, it has become a promising target for the treatment of impaired cognition. Acupuncture at the Baihui (DU20) and Shenting (DU24) acupoints is commonly used in China to clinically treat post‑stroke cognitive impairment; however, the precise mechanism of its action is largely unknown. In the present study, we evaluated the therapeutic efficacy of electroacupuncture against post-stroke cognitive impairment and investigated the underlying molecular mechanisms using a rat model of focal cerebral ischemia-reperfusion (I/R) injury. Electroacupuncture at Baihui and Shenting was identified to significantly ameliorate neurological deficits and reduce cerebral infarct volume. Additionally, electroacupuncture improved learning and memory ability in cerebral I/R injured rats, demonstrating its therapeutic efficacy against post-stroke cognitive impairment. Furthermore, electroacupuncture significantly suppressed the I/R-induced activation of NF-κB signaling in ischemic cerebral tissues. The inhibitory effect of electroacupuncture on NF-κB activation led to the inhibition of cerebral cell apoptosis. Finally, electroacupuncture markedly downregulated the expression of pro-apoptotic Bax and Fas, two critical downstream target genes of the NF-κB pathway. Collectively, our findings suggest that inhibition of NF-κB‑mediated neuronal cell apoptosis may be one mechanism via which electroacupuncture at Baihui and Shenting exerts a therapeutic effect on post-stroke cognitive impairment.
authors.affiliation: College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, PR China.
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Feng
authors.forename: Shanli
authors.initials: S
authors.lastname: Yang
authors.forename: Jiao
authors.initials: J
authors.lastname: Liu
authors.forename: Jia
authors.initials: J
authors.lastname: Huang
authors.forename: Jun
authors.initials: J
authors.lastname: Peng
authors.forename: Jiumao
authors.initials: J
authors.lastname: Lin
authors.forename: Jing
authors.initials: J
authors.lastname: Tao
authors.forename: Lidian
authors.initials: L
authors.lastname: Chen
mesh_terms: D015669:Acupuncture Points; D000818:Animals; D017209:Apoptosis; D002545:Brain Ischemia / Q000150:complications / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D002467:Cell Nucleus / Q000378:metabolism; D002544:Cerebral Infarction; D003072:Cognition Disorders / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D015536:Down-Regulation; D015671:Electroacupuncture; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D021381:Protein Transport; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D015398:Signal Transduction; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism; D019014:fas Receptor / Q000235:genetics / Q000378:metabolism
chemical_list: C491898:Fas protein, rat; D016328:NF-kappa B; D051028:bcl-2-Associated X Protein; D019014:fas Receptor