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Electroacupuncture potentiates peripheral CB2 receptor-inhibited chronic pain in a mouse model of knee osteoarthritis

Authors Yuan X, Wang Q, Su W, Li HP, Wu CH, Gao F, Xiang HC, Zhu H, Lin LX, Hu XF, Cao J, Li JJ, Li M

Received 19 April 2018

Accepted for publication 10 August 2018

Published 8 November 2018 Volume 2018:11 Pages 2797—2808


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Katherine Hanlon

Xiao-Cui Yuan,1 Qiang Wang,2 Wen Su,3 Hong-Ping Li,1 Cai-Hua Wu,3 Fang Gao,1 Hong-Chun Xiang,1 He Zhu,1 Li-Xue Lin,1 Xue-Fei Hu,1 Jie Cao,4 Jing-Jing Li,1 Man Li1

1Department of Neurobiology and Key Laboratory of Neurological Diseases of Ministry of Education, The Institute of Brain Research, School of Basic Medicine, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, People’s Republic of China; 2Department of Anesthesiology, First Affiliated Hospital of Xi’an JiaoTong University, Xi’an, People’s Republic of China; 3Department of Acupuncture, Wuhan First Hospital, Wuhan 430030, People’s Republic of China; 4Department of Neurology, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, People’s Republic of China

Knee osteoarthritis (KOA) is a highly prevalent, chronic joint disorder, with chronic pain as its typical symptom. Although studies have shown that an activated peripheral CB2 receptor can reduce acute pain, whether the CB2 receptor is involved in electroacupuncture (EA) inhibiting chronic pain and the involved mechanism remains unclear. The aim of this study was to investigate whether EA may strengthen peripheral CB2 receptor-inhibited chronic pain in a mouse model of KOA.
Materials and methods: KOA was induced by intra-articular injection of monosodium iodoacetate (MIA) into the left knee joint of mice. Thermal hyperalgesia was tested with the hot plate test, and mechanical allodynia was quantified using von Frey filaments. The expression of CB2 receptor and IL-1β were quantified by using immunofluorescence labeling.
Results: EA treatment at 2 Hz+1 mA significantly increased the expression of CB2 receptor in fibroblasts and decreased the expression of IL-1β in the menisci compared with that in the KOA group. However, EA had no effect on the expression of IL-1β in CB2−/− mice. At 2 Hz+1 mA, EA significantly increased mechanical threshold, thermal latency, and weight borne after KOA modeling. However, knockout of the CB2 receptor blocked these effects of EA. After 2 Hz+1 mA treatment, EA significantly reduced the Osteoarthritis Research Society International (OARSI) score after KOA modeling. However, EA had no significant effect on the OARSI score in CB2−/− mice.
Conclusion: EA reduced the expression of IL-1β by activating the CB2 receptor, thus inhibiting the chronic pain in the mouse model of KOA.

Keywords: cannabinoid, acupuncture, inflammatory pain, IL-1β

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