口腔医学研究 ›› 2018, Vol. 34 ›› Issue (11): 1244-1248.DOI: 10.13701/j.cnki.kqyxyj.2018.11.023

• 颞下颌关节研究 • 上一篇    下一篇

三叉神经节TLR4-MyD88信号通路参与大鼠颞下颌关节炎症诱发的神经免疫反应

李维佳1,2, 李路佳1, 樊帆1, 金海威1*   

  1. 1. 大连医科大学口腔医学院 辽宁 大连 116044;
    2. 呼伦贝尔市人民医院口腔内科 内蒙古 呼伦贝尔 021008
  • 收稿日期:2018-06-15 出版日期:2018-11-28 发布日期:2018-11-23
  • 通讯作者: 金海威,E-mail:1760684062@qq.com
  • 作者简介:李维佳(1992~ ),女,内蒙古人,硕士,主要从事口腔颌面部疼痛的医学研究,现就职于呼伦贝尔市人民医院口腔内科。

TLR4-MyD88 Signal Pathway in Trigeminal Ganglia Involved in Immunoreactivity Induced by Temporomandibular Joint Inflammation in Rats

LI Wei-jia1,2,LI Lu-jia1, FAN Fan1, JIN Hai-wei1*   

  1. 1. School of Stomatology, Dalian Medical University, Dalian 116044, China;
    2.Department of Oral Medicine, HulunBuir People's Hospital,Hulunbeier 021008,China.
  • Received:2018-06-15 Online:2018-11-28 Published:2018-11-23

摘要: 目的:利用大鼠颞下颌关节炎症(temporomandibular joint inflammation,TMJI)模型,检测Toll样受体4 (Toll-like receptor 4,TLR4)及其信号通路在三叉神经节中的动态表达,探究神经系统TLR4信号通路在TMJI及疼痛反应中的作用。方法:颞下颌关节下腔注射完全弗氏佐剂法建立大鼠TMJI动物模型,应用苏木精-伊红(hematoxylin-eosin staining,HE)染色法观察TMJI进展,免疫组织化学染色法检测三叉神经节中TLR4与髓样分化因子88(myeloid differentiation primary response gene 88,MyD88)的表达变化。结果:完全弗氏佐剂诱发TMJI后,三叉神经节神经元TLR4与MyD88的表达显著增加,且两者表达呈低度相关性。结论:三叉神经节 TLR4-MyD88信号通路参与TMJI诱发的神经免疫反应,神经元TLR4的激活可能通过MyD88依赖途径进行信号转导。

关键词: 颞下颌关节炎症, Toll样受体4, 髓样分化因子88, 神经免疫反应

Abstract: Objective: To investigate the dynamic expression of TLR4 and its signal pathway in trigeminal ganglia (TG) by using a temporomandibular joint inflammation (TMJI) animal model in rats, and further to explore the role of TLR4 signal pathway involved in the neural immune response during process of TMJI and accompanied pain. Methods: Rats model of TMJI were established by intra-articular injection of Freund's adjuvant complete. Histopathological examination showed the progressive pathological changes in the TMJ were detected by HE staining, and the expression of TLR4 or MyD88 in TG were observed by immunohistochemistry. Results: The expression of TLR4 and MyD88 in TG increased significantly post TMJI. Correlation analysis showed low correlation between TLR4 and MyD88 expression. Conclusion: TLR4-MyD88 signal pathway in TG involved in neural immune response during TMJI. The signal transduction of activation of TLR4 in neurons may be mediated by MyD88 dependent pathway.

Key words: Temporomandibular joint inflammation, TLR4, MyD88, Neural immune response