{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:46:29Z","timestamp":1786977989977,"version":"build-2736575974"},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2023,10,16]],"date-time":"2023-10-16T00:00:00Z","timestamp":1697414400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2024,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Neuropathic pain (NP) is mainly caused by lesions or diseases of the somatosensory nervous system and triggers severe physical burdens to patients. It is claimed that activated microglia\u2010mediated neuroinflammation participates in the development of NP, which is regulated by p38 mitogen\u2010activated protein kinase (MAPK)\/nuclear factor\u2010\u03baappa B (NF\u2010\u03baB) p65 signaling. G protein\u2010coupled receptor 39 (GPR39) is a trans\u2010membrane protein involved in the activation of cellular transduction pathways, and TC\u2010G 1008, a GPR39 agonist, is believed to have inhibitory effects on neuroinflammation. Our study will explore the possible alleviatory function of TC\u2010G 1008 on NP in a rat model. GPR39 was found markedly downregulated in the spinal dorsal horn of chronic constriction injury (CCI)\u2010stimulated rats. Rats were treated with CCI, followed by intranasal administration with 7.5 and 15\u2009mg\/kg TC\u2010G 1008 at 1, 25, 49, and 73\u2009h postmodeling, respectively. Drastically lowered values of paw withdrawal threshold and paw withdrawal latency, upregulated ionized calcium\u2010binding adapter molecule 1, increased release of inflammatory cytokines, elevated spinal malondialdehyde levels, and reduced spinal glutathione peroxidase levels were observed in CCI\u2010stimulated rats, all of which were markedly alleviated and rescued by TC\u2010G 1008. Furthermore, the levels of p\u2010p38\/p38 and p\u2011NF\u2011\u03baB p65 were found signally repressed in the spinal dorsal horn of CCI\u2010stimulated rats, which was notably reversed by TC\u2010G 1008. Collectively, TC\u2010G 1008 markedly alleviated NP and neuroinflammation in CCI\u2010treated rats. Our findings provide an attractive future direction for the treatment of NP.<\/jats:p>","DOI":"10.1002\/jbt.23545","type":"journal-article","created":{"date-parts":[[2023,10,16]],"date-time":"2023-10-16T05:23:52Z","timestamp":1697433832000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Activation of G protein\u2010coupled receptor 39 alleviates neuropathic pain and chronic inflammation"],"prefix":"10.1002","volume":"38","author":[{"given":"Fang","family":"Cheng","sequence":"first","affiliation":[{"name":"Department of Anesthesiology and Pain Clinic The Affiliated Lianyungang Oriental Hospital of Kangda College of Nanjing Medical University Lianyungang China"},{"name":"Department of Oncology The Affiliated Lianyungang Oriental Hospital of Xuzhou Medical University Lianyungang 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