Author: Liao HY1,2, Hsieh CL1,3,4,5, Huang CP6, Lin YW7,8
Affiliation:
1College of Chinese Medicine, Graduate Institute of Acupuncture Science, China Medical University, Taichung, 40402, Taiwan.
2Department of Acupuncture, China Medical University Hospital, 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.
6Research Center for Chinese Medicine & Acupuncture, China Medical University, Taichung, 40402, Taiwan. agustacagiva@yahoo.com.tw.
7College of Chinese Medicine, Graduate Institute of Acupuncture Science, China Medical University, Taichung, 40402, Taiwan. yiwenlin@mail.cmu.edu.tw.
8Research Center for Chinese Medicine & Acupuncture, China Medical University, Taichung, 40402, Taiwan. yiwenlin@mail.cmu.edu.tw.
Conference/Journal: Sci Rep.
Date published: 2017 Nov 15
Other:
Volume ID: 7 , Issue ID: 1 , Pages: 15679 , Special Notes: doi: 10.1038/s41598-017-16031-y. , Word Count: 213
Although inflammatory pain is a common clinical condition, its mechanisms are still unclear. Electroacupuncture (EA), a well-known method of pain management, may reduce inflammatory pain by regulating neurons, astrocytes, and inflammatory signaling pathways. Injections of complete Freund's adjuvant (CFA), which can initiate cell-mediated inflammatory pain, resulted in significant hyperalgesia, which was subsequently prevented by EA. In CFA-injected mice, a dramatic increase was observed in the expression of the following proteins in the dorsal root ganglion and spinal cord dorsal horn: the astrocytic marker GFAP, S100B, RAGE, pPKCε, COX-2, pERK, and pNFκB. These effects were reversed by EA. In addition, mechanical hyperalgesia was significantly reduced in the N6-cyclopentyladenosine (CPA) i.p. or i.m. and endomorphin (EM) i.p. groups. Neither EM i.m. nor EM i.p. exhibited any analgesic effect on thermal hyperalgesia. However, both CPA i.m. and CPA i.p. attenuated thermal hyperalgesia in the mouse inflammatory pain model. We showed that CPA reduced COX-2 and pPKCε expression. However, EM administration did not reduce COX-2 levels. Combined administration of naloxone and rolofylline increased pPKCε and COX-2 pathways. Taken together, our study results revealed a novel and detailed mechanism of EA-induced analgesia that involves the regulation of the opioid and adenosine pathways.
PMID: 29142219 DOI: 10.1038/s41598-017-16031-y
