期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 82, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.intimp.2020.106355
关键词
Inflammatory pain; Microglial activation; Muscone; NOX4; JAK2-STAT3 pathway; NLRP3
资金
- Perioperative Organ Protection Research Engineering Center [N2018C020]
- Ministry of Health of Jilin Province [2016Q017]
Previous studies have shown that muscone, a pharmacologically active ingredient isolated from musk, has excellent effects on anti-inflammation. However, its effect on microglia activation-induced inflammatory pain is not known yet. In the present study, a mouse BV2 microglia cell activation-mediated inflammatory model was developed with LPS induction, and a mouse inflammatory pain model was established with CFA injection. The inhibitory effect of muscone on microglia inflammatory activation was verified by measuring pro-inflammatory cytokines expression (interleukin-6, tumor necrosis factor-alpha, and interleukin-1 beta; IL-6, TNF-alpha and IL-1 beta). We found that muscone suppressed microglial activation-mediated inflammatory response through the NADPH oxidase 4 (NOX4)/janus kinase 2-signal transducer and activator of transcription 3 (JAK2-STAT3) pathway and pyrin-domain-containing 3 (NLRP3) inflammasome. Notably, muscone mitigated CFA-induced pain hypersensitivity and inflammation, as well as microglia cell activation in vivo. Furthermore, muscone inhibited the CFA-induced NOX4, p-JAK2/p-STAT3, and NLRP3 inflammasome expression in spinal cord of mice. In conclusion, this study uncovered that muscone relieved inflammatory pain by inhibiting microglial activation-mediated inflammatory response via abrogation of the NOX4/JAK2-STAT3 pathway and NLRP3 inflammasome. This finding of muscone is promising for treating inflammatory pain.
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