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作 者:Longqing Zhang Xi Tan Fanhe Song Danyang Li Jiayi Wu Shaojie Gao Jia Sun Daiqiang Liu Yaqun Zhou Wei Mei
出 处:《Neural Regeneration Research》2024年第3期687-696,共10页中国神经再生研究(英文版)
基 金:supported by the National Notural Science Foundation of China,Nos.82071556 and 82271291 (both to WM)
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 unclear.In 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 rats.Intrathecal 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 neuroinflammation.These changes were abolished by GPR39 small interfering RNA(siRNA),Ex-527(SIRT1 inhibitor),and PGC-1αsiRNA.Taken together,these findings show that GPR39 activation ameliorates mechanical allodynia by activating the SIRT1/PGC-1αpathway in rats with spared nerve injury.
关 键 词: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)
分 类 号:R741[医药卫生—神经病学与精神病学] R-332[医药卫生—临床医学]
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