IL-1β在大鼠颞下颌关节炎性痛中的作用机制探讨  被引量:3

The mechanism of IL-1β contributing to temporomandibular joint inflammatory pain in rats

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作  者:潘洪祥[1] 孙伟[1] 袁荣涛[1] 张鹏[1] 邱建忠[1] PAN Hong-xiang;SUN Wei;YUAN Rong-tao;ZHANG Peng;QIU Jian-zhong(Department of Stomatology,Qindao Municipal Hospital Affiliated to Qingdao University,Qingdao 266000,Shangdong Province,China)

机构地区:[1]青岛大学附属青岛市市立医院,口腔医学中心,山东青岛266000

出  处:《中国口腔颌面外科杂志》2020年第5期401-406,共6页China Journal of Oral and Maxillofacial Surgery

基  金:山东省自然科学基金(ZR2016HM34);青岛大学附属青岛市市立医院博士科研启动经费(Ⅷ院博201832)。

摘  要:目的 :探讨ERK1/2、NF-κB信号通路是否参与白细胞介素1β(IL-1β)上调疼痛因子Nav1.7的表达,进而参与大鼠颞下颌关节炎性痛。方法:建立颞下颌关节炎症模型或通过大鼠三叉神经节脑立体定位实验,于活体大鼠三叉神经节内注射IL-1β,评估三叉神经节p-ERK1/2、p-p65、Nav1.7、COX-2、p-CREB等分子的表达及摆头阈值变化。体外培养大鼠三叉神经节,IL-1β单独或联合ERK、NF-κB抑制剂U0126、PDTC,利用实时定量PCR及蛋白免疫印迹评估三叉神经节p-ERK1/2、p-p65、Nav1.7、COX-2、p-CREB的表达变化。采用SPSS 22.0软件包进行数据统计。结果:诱导颞下颌关节炎症24 h及活体大鼠三叉神经节内注射IL-1β24 h后,三叉神经节内p-ERK1/2、p-p65、Nav1.7、COX-2、p-CREB表达显著上调,同时摆头阈值降低。ERK及NF-κB抑制剂均可阻断IL-1β上调三叉神经节内Nav1.7、COX-2、p-CREB表达。结论:IL-1β通过ERK1/2、NF-κB信号通路上调三叉神经节内Nav1.7的表达,进而参与大鼠颞下颌关节炎性痛。PURPOSE: To investigate whether the ERK1/2 and NF-κB signaling pathways are involved in interleukin-1 beta(IL-1β) up-regulation of Nav1.7 expression and then participate in temporomandibular joint(TMJ) inflammatory pain in rats. METHODS: TMJ nociception and the expressions of p-ERK1/2, p-p65, Nav1.7, COX-2, and p-CREB were evaluated after inducing of TMJ inflammation or microinjecting of IL-1β into the trigeminal ganglion(TG). Rats TG explants were treated with IL-1β with or without inhibitors, including U0126 for ERK and PDTC for NF-κB, and then the gene expressions were evaluated using real-time PCR and Western blot assays. Statistical analysis was performed using SPSS 22.0 software package. RESULTS: TMJ inflammation or microinjection of IL-1β into the TG for 24 h both induced TMJ pain and correspondingly up-regulated p-ERK1/2, p-p65, Nav1.7, COX-2, and p-CREB expressions. Both U0126 and PDTC blocked IL-1β up-regulation of Nav1.7, COX-2, p-CREB expressions in TG explants. CONCLUSIONS: IL-1β up-regulates Nav1.7 expression through ERK1/2 and NF-κB signaling pathways, and then contributes to TMJ inflammatory pain in rats.

关 键 词:IL-1Β ERK1/2 NF-ΚB Nav1.7 颞下颌关节炎性痛 

分 类 号:R782.6[医药卫生—口腔医学]

 

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