Activation of mitogen-activated protein kinases in satellite glial cells of the trigeminal ganglion contributes to substance P-mediated inflammatory pain

作     者：Yanyan Zhang Ning Song Fei Liu Jiu Lin Mengke Liu Chaolan Huang Daqing Liao Cheng Zhou Hang Wang Jiefei Shen 

作者机构：State Key Laboratory of Oral DiseasesNational Clinical Research Center for Oral DiseasesWest China Hospital of StomatologySichuan UniversityChengduChina West China School of Stomatology Sichuan UniversityChengduChina Laboratory of Anesthesia & Critical Care MedicineTranslational Neuroscience CenterWest China Hospital of Sichuan UniversityChengduChina 

出 版 物：《International Journal of Oral Science》 (国际口腔科学杂志（英文版）)

年 卷 期：2019年第11卷第3期

页      面：213-222页

核心收录：

学科分类：10[医学] 

基　　金：supported by the National Natural Science Foundation of China (Grant No. 81870800) the Science and Technology Department of Sichuan Province (Grant No. 2015JY0146) 

主　　题：glial closely related tumor necrosis factor 

摘      要：Inflammatory orofacial pain,in which substance P (SP) plays an important role,is closely related to the cross-talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs).SGC activation is emerging as the key mechanism underlying inflammatory pain through different signalling mechanisms,including glial fibrillary acidic protein (GFAP) activation,phosphorylation of mitogen-activated protein kinase (MAPK) signalling pathways,and cytokine ***,in the TG,the mechanism underlying SP-mediated orofacial pain generated by SGCs is largely *** this study,we investigated whether SP is involved in inflammatory orofacial pain by upregulating interleukin (IL)-1β and tumour necrosis factor (TNF)-α from SGCs,and we explored whether MAPK signalling pathways mediate the pain *** the present study,complete Freund’s adjuvant (CFA) was injected into the whisker pad of rats to induce an inflammatory model in *** was administered to SGC cultures in vitro to confirm the effect of *** expression analysis showed that pre-injection of L703,606 (an NK-1 receptor antagonist),U0126 (an inhibitor of MAPK/extracellular signal-regulated kinase [ERK] kinase [MEK] 1/2),and SB203580 (an inhibitor of P38) into the TG to induce targeted prevention of the activation of the NK-1 receptor and the phosphorylation of MAPKs significantly suppressed CFA-induced inflammatory *** addition,SP promoted SGC activation,which was proven by increased GFAP,p-MAPKs,IL-1β and TNF-α in SGCs under inflammatory ***,the increase in IL-1β and TNF-α was suppressed by L703,606,U0126 and SB203580 in vivo and in *** present findings suggested that SP,released from TG neurons,activated SGCs through the ERK1/2 and P38 pathways and promoted the production of IL-1β and TNF-α from SGCs,contributing to inflammatory orofacial pain associated with peripheral sensitization.