脂多糖对大鼠三叉神经节Nav1.7表达的调控及机制研究  

The mechanism of lipopolysaccharide upregulating trigeminal ganglionic sodium channel 1.7 expression in rats

作　　者：闫婷婷 张静[2] 庄立琨 王莉莉[2] 张鹏[2,3] 袁荣涛[2] YAN Ting-ting;ZHANG Jing;ZHUANG Li-kun;WANG Li-li;ZHANG Peng;YUAN Rong-tao(College of Stomatology,Qingdao University,Qingdao 266003,Shandong Province;Department of Stomatology,Qingdao Hospital,University of Health and Rehabilitation Sciences(Qingdao Municipal Hospital),Qingdao 266071,Shandong Province;Department of Oral&Maxillofacial Surgery,Peking University School and Hospital of Stomatology,Beijing 100081,China)

机构地区：[1]青岛大学口腔医学院,山东青岛266003 [2]康复大学青岛医院(青岛市市立医院)口腔医学中心,山东青岛266071 [3]北京大学口腔医学院口腔颌面外科,北京100081

出　　处：《中国口腔颌面外科杂志》2023年第4期345-351,共7页China Journal of Oral and Maxillofacial Surgery

基　　金：山东省自然科学基金(ZR2016HM34)。

摘　　要：目的:探讨脂多糖(LPS)是否及如何上调大鼠三叉神经节(TG)内Nav1.7的表达,从而调控大鼠颞下颌关节(TMJ)炎性痛。方法:选择成年雄性SD大鼠,应用大鼠三叉神经节脑立体定位实验,于活体大鼠TG内微量注射LPS,观察大鼠摆头阈值的变化,并检测TG内Nav1.7的表达。将大鼠TG进行体外离体培养,LPS单独或联合卫星胶质细胞(SGC)活化抑制剂fluorocitrate(FC)、NF-κB抑制剂PDTC进行处理。应用实时定量PCR、Western免疫印迹实验检测TG内Nav1.7、p-p65、GFAP等分子的表达变化。采用SPSS 22.0软件包对数据进行统计学分析。结果:活体大鼠TG内微量注射LPS 24 h后,TG内Nav1.7的表达显著上调且大鼠摆头阈值降低。SGC活化抑制剂FC可阻断LPS上调的TG内Nav1.7的表达,NF-κB抑制剂PDTC可阻断LPS上调的TG内p-p65、GFAP及Nav1.7的表达。结论:LPS可能通过NF-κB信号通路(p-p65)激活三叉神经节内的卫星胶质细胞,进而上调神经元内Nav1.7的表达,从而调控大鼠颞下颌关节炎性痛。PURPOSE:To investigate whether and how lipopolysaccharide(LPS)upregulates the expression of sodium channel 1.7(Nav1.7)in trigeminal ganglion(TG),and then participate in temporomandibular joint(TMJ)inflammatory pain in rats.METHODS:Through microinjection of LPS into the TG in adult male Sprague-Dawley(SD)rats,rats'head withdrawal threshold was observed and the expression of Nav1.7 in TG was detected.After culturing rats TG explants in vitro,the rats TG explants were treated with LPS with or without inhibitors,including fluorocitrate(FC)for satellite glial cell(SGC)activation and pyrrolidinedithiocarbamate(PDTC)for NF-κB,and then the expression changes of Nav1.7,p-p65 and GFAP in TG was detected using real-time PCR and Western blot assays.SPSS 22.0 software package was used for data analysis.RESULTS:Nav1.7 expression was significantly upregulated in the TG and the head withdrawal threshold was reduced after microinjection of LPS into the TG for 24 h.LPS-induced upregulation of Nav1.7 expression in the TG was blocked by SGC activation inhibitor FC.LPS-induced upregulation of p-p65,GFAP and Nav1.7 expressions in the TG were blocked by NF-κB inhibitor PDTC.CONCLUSIONS:LPS upregulates the expression of Nav1.7 through NF-κB signaling pathway(p-p65)activating satellite glial cell(SGC)of trigeminal ganglion,and then participates in TMJ inflammatory pain in rats.

关 键 词：脂多糖 三叉神经节 卫星胶质细胞 钠离子通道1.7 颞下颌关节炎性痛 

分 类 号：R782.6[医药卫生—口腔医学]