Activation of G-protein-coupled receptor 39 reduces neuropathic pain in a rat model
作者机构:Department of AnesthesiologyHubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Healthand Wuhan Clinical Research Center for Geriatric AnesthesiaTongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei ProvinceChina
出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))
年 卷 期:2024年第19卷第3期
页 面:687-696页
核心收录:
学科分类:0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100204[医学-神经病学] 10[医学]
基 金:supported by the National Notural Science Foundation of China Nos.82071556 and 82271291 (both to WM)
主 题:G-protein-coupled receptor 39(GPR39) neuroinflammation neuropathic pain nuclear respiratory factor 1(NRF1) peroxisome proliferator-activated receptor-γcoactivator 1α(PGC-1α) sirtuin 1(SIRT1) spinal cord mitochondrial transcription factor A(TFAM)
摘 要:Activated G-protein-coupled receptor 39(GPR39)has been shown to attenuate inflammation by interacting with sirtuin 1(SIRT1)and peroxisome proliferator-activated receptor-γcoactivator 1α(PGC-1α).However,whether GPR39 attenuates neuropathic pain remains *** this study,we established a Sprague-Dawley rat model of spared nerve injury-induced neuropathic pain and found that GPR39 expression was significantly decreased in neurons and microglia in the spinal dorsal horn compared with sham-operated *** injection of TC-G 1008,a specific agonist of GPR39,significantly alleviated mechanical allodynia in the rats with spared nerve injury,improved spinal cord mitochondrial biogenesis,and alleviated *** changes were abolished by GPR39 small interfering RNA(siRNA),Ex-527(SIRT1 inhibitor),and PGC-1α*** together,these findings show that GPR39 activation ameliorates mechanical allodynia by activating the SIRT1/PGC-1αpathway in rats with spared nerve injury.