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

被引:27
|
作者
Yuan, Xiao-Cui [1 ,2 ]
Wang, Qiang [3 ]
Su, Wen [4 ]
Li, Hong-Ping [1 ,2 ]
Wu, Cai-Hua [4 ]
Gao, Fang [1 ,2 ]
Xiang, Hong-Chun [1 ,2 ]
Zhu, He [1 ,2 ]
Lin, Li-Xue [1 ,2 ]
Hu, Xue-Fei [1 ,2 ]
Cao, Jie [5 ]
Li, Jing-Jing [1 ,2 ]
Li, Man [1 ,2 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Basic Med, Inst Brain Res,Minist Educ,Dept Neurobiol, Wuhan 430030, Hubei, Peoples R China
[2] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Basic Med, Key Lab Neurol Dis,Minist Educ,Inst Brain Res, Wuhan 430030, Hubei, Peoples R China
[3] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Anesthesiol, Xian, Shaanxi, Peoples R China
[4] Wuhan First Hosp, Dept Acupuncture, Wuhan 430030, Hubei, Peoples R China
[5] Huazhong Univ Sci & Technol, Tongji Hosp, Dept Neurol, Tongji Med Coll, Wuhan 430030, Hubei, Peoples R China
来源
JOURNAL OF PAIN RESEARCH | 2018年 / 11卷
基金
中国国家自然科学基金;
关键词
cannabinoid; acupuncture; inflammatory pain; IL-1; beta; CANNABINOID RECEPTORS; ENDOCANNABINOID SYSTEM; EXPRESSION; MICE; RAT; AGONIST; ACUPUNCTURE; STIMULATION; FIBROBLASTS; ACTIVATION;
D O I
10.2147/JPR.S171664
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Purpose: 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-1 beta 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-1 beta in the menisci compared with that in the KOA group. However, EA had no effect on the expression of IL-1 beta 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-1 beta by activating the CB2 receptor, thus inhibiting the chronic pain in the mouse model of KOA.
引用
收藏
页码:2797 / 2808
页数:12
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