【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。更多还原

【Abstract】 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.更多还原