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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 924541, 15 pages
http://dx.doi.org/10.1155/2013/924541
Research Article

Electroacupuncture Could Regulate the NF- B Signaling Pathway to Ameliorate the Inflammatory Injury in Focal Cerebral Ischemia/Reperfusion Model Rats

1Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
2Chongqing Key Laboratory of Neurology, 1 Youyi Road, Yuzhong District, Chongqing 400016, China
3Department of Neurology, Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan Province 64600, China
4Department of Oncology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China

Received 23 January 2013; Revised 10 June 2013; Accepted 18 June 2013

Academic Editor: Lijun Bai

Copyright © 2013 Wen-yi Qin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The activated nuclear factor-KappaB signaling pathway plays a critical role in inducing inflammatory injury. It has been reported that electroacupuncture could be an effective anti-inflammatory treatment. We aimed to explore the complex mechanism by which EA inhibits the activation of the NF-κB signal pathway and ameliorate inflammatory injury in the short term; the effects of NEMO Binding Domain peptide for this purpose were compared. Focal cerebral I/R was induced by middle cerebral artery occlusion for 2 hrs. Total 380 male Sprague-Dawley rats are in the study. The neurobehavioral scores, infarction volumes, and the levels of IL-1β and IL-13 were detected. NF-κB p65, IκBα, IKKα, and IKKβ were analyzed and the ability of NF-κB binding DNA was investigated. The EA treatment and the NBD peptide treatment both reduced infarct size, improved neurological scores, and regulated the levels of IL-1β and IL-13. The treatment reduced the expression of IKKα and IKKβ and altered the expression of NF-κB p65 and IκBα in the cytoplasm and nucleus; the activity of NF-κB was effectively reduced. We conclude that EA treatment might interfere with the process of NF-κB nuclear translocation. And it also could suppress the activity of NF-κB signaling pathway to ameliorate the inflammatory injury after focal cerebral ischemia/reperfusion.