| http://purl.uniprot.org/citations/37842769 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/37842769 | http://www.w3.org/2000/01/rdf-schema#comment | "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-mediated neuroinflammation participates in the development of NP, which is regulated by p38 mitogen-activated protein kinase (MAPK)/nuclear factor-κappa B (NF-κB) p65 signaling. G protein-coupled receptor 39 (GPR39) is a trans-membrane protein involved in the activation of cellular transduction pathways, and TC-G 1008, a GPR39 agonist, is believed to have inhibitory effects on neuroinflammation. Our study will explore the possible alleviatory function of TC-G 1008 on NP in a rat model. GPR39 was found markedly downregulated in the spinal dorsal horn of chronic constriction injury (CCI)-stimulated rats. Rats were treated with CCI, followed by intranasal administration with 7.5 and 15 mg/kg TC-G 1008 at 1, 25, 49, and 73 h postmodeling, respectively. Drastically lowered values of paw withdrawal threshold and paw withdrawal latency, upregulated ionized calcium-binding adapter molecule 1, increased release of inflammatory cytokines, elevated spinal malondialdehyde levels, and reduced spinal glutathione peroxidase levels were observed in CCI-stimulated rats, all of which were markedly alleviated and rescued by TC-G 1008. Furthermore, the levels of p-p38/p38 and p-NF-κB p65 were found signally repressed in the spinal dorsal horn of CCI-stimulated rats, which was notably reversed by TC-G 1008. Collectively, TC-G 1008 markedly alleviated NP and neuroinflammation in CCI-treated rats. Our findings provide an attractive future direction for the treatment of NP."xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.org/dc/terms/identifier | "doi:10.1002/jbt.23545"xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/author | "Cheng F."xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/author | "Liu J."xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/author | "Ma J."xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/author | "Yang A."xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/author | "Yan F."xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/date | "2024"xsd:gYear |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/name | "J Biochem Mol Toxicol"xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/pages | "e23545"xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/title | "Activation of G protein-coupled receptor 39 alleviates neuropathic pain and chronic inflammation."xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://purl.uniprot.org/core/volume | "38"xsd:string |
| http://purl.uniprot.org/citations/37842769 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/37842769 |
| http://purl.uniprot.org/citations/37842769 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/37842769 |
| http://purl.uniprot.org/uniprot/#_A0A8J8Y1V6-mappedCitation-37842769 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37842769 |
| http://purl.uniprot.org/uniprot/#_A6QR73-mappedCitation-37842769 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/37842769 |
| http://purl.uniprot.org/uniprot/A6QR73 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/37842769 |
| http://purl.uniprot.org/uniprot/A0A8J8Y1V6 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/37842769 |