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BioMed Research International
Volume 2017 (2017), Article ID 5068347, 8 pages
https://doi.org/10.1155/2017/5068347
Research Article

Role of Transient Receptor Potential Vanilloid 1 in Electroacupuncture Analgesia on Chronic Inflammatory Pain in Mice

1Department of Acupuncture, China Medical University Hospital, Taichung 40402, Taiwan
2College of Chinese Medicine, Graduate Institute of Acupuncture Science, China Medical University, Taichung 40402, Taiwan
3College of Chinese Medicine, Graduate Institute of Integrated Medicine, China Medical University, Taichung 40402, Taiwan
4Department of Chinese Medicine, China Medical University Hospital, Taichung 40402, Taiwan
5Research Center for Chinese Medicine & Acupuncture, China Medical University, Taichung 40402, Taiwan

Correspondence should be addressed to Yi-Wen Lin

Received 13 August 2017; Accepted 21 November 2017; Published 12 December 2017

Academic Editor: Jane Hanrahan

Copyright © 2017 Jun Yang 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

Chronic inflammatory pain may result from peripheral tissue injury or inflammation, increasing the release of protons, histamines, adenosine triphosphate, and several proinflammatory cytokines and chemokines. Transient receptor potential vanilloid 1 (TRPV1) is known to be involved in acute to subacute neuropathic and inflammatory pain; however, its exact mechanisms in chronic inflammatory pain are not elucidated. Our results showed that EA significantly reduced chronic mechanical and thermal hyperalgesia in the chronic inflammatory pain model. Chronic mechanical and thermal hyperalgesia were also abolished in TRPV1−/− mice. TRPV1 increased in the dorsal root ganglion (DRG) and spinal cord (SC) at 3 weeks after CFA injection. The expression levels of downstream molecules such as pPKA, pPI3K, and pPKC increased, as did those of pERK, pp38, and pJNK. Transcription factors (pCREB and pNFκB) and nociceptive ion channels (Nav1.7 and Nav1.8) were involved in this process. Inflammatory mediators such as GFAP, S100B, and RAGE were also involved. The expression levels of these molecules were reduced in EA and TRPV1−/− mice but not in the sham EA group. Our data provided evidence to support the clinical use of EA for treating chronic inflammatory pain.