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外周速激肽NK1受体在角叉菜胶诱导的大鼠颞下颌关节炎症中的作用

Participation of peripheral tachykinin NK1 receptors in the carrageenan-induced inflammation of the rat temporomandibular joint.

作者信息

Denadai-Souza Alexandre, Camargo Livia de Lucca, Ribela Maria T C P, Keeble Julie E, Costa Soraia K P, Muscará Marcelo N

机构信息

Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-900, SP, Brazil.

出版信息

Eur J Pain. 2009 Sep;13(8):812-9. doi: 10.1016/j.ejpain.2008.09.012. Epub 2008 Oct 31.

DOI:10.1016/j.ejpain.2008.09.012
PMID:18976941
Abstract

Temporomandibular disorders represent one of the major challenges in dentistry therapeutics. This study was undertaken to evaluate the time course of carrageenan-induced inflammation in the rat temporomandibular joint (TMJ) and to investigate the role of tachykinin NK(1) receptors. Inflammation was induced by a single intra-articular (i.art.) injection of carrageenan into the left TMJ (control group received sterile saline). Inflammatory parameters such as plasma extravasation, leukocyte influx and mechanical allodynia (measured as the head-withdrawal force threshold) and TNFalpha and IL-1beta concentrations were measured in the TMJ lavages at selected time-points. The carrageenan-induced responses were also evaluated after treatment with the NK(1) receptor antagonist SR140333. The i.art. injection of carrageenan into the TMJ caused a time-dependent plasma extravasation associated with mechanical allodynia, and a marked neutrophil accumulation between 4 and 24h. Treatment with SR140333 substantially inhibited the increase in plasma extravasation and leukocyte influx at 4 and 24h, as well as the production of TNFalpha and IL-1beta into the joint cavity, but failed to affect changes in head-withdrawal threshold. The results obtained from the present TMJ-arthritis model provide, for the first time, information regarding the time course of this experimental inflammatory process. In addition, our data show that peripheral NK(1) receptors mediate the production of both TNFalpha and IL-1beta in the TMJ as well as some of the inflammatory signs, such as plasma extravasation and leukocyte influx, but not the nociceptive component.

摘要

颞下颌关节紊乱是牙科治疗中的主要挑战之一。本研究旨在评估角叉菜胶诱导的大鼠颞下颌关节(TMJ)炎症的时间进程,并研究速激肽NK(1)受体的作用。通过向左侧TMJ单次关节内(i.art.)注射角叉菜胶诱导炎症(对照组注射无菌生理盐水)。在选定的时间点测量TMJ灌洗液中的炎症参数,如血浆外渗、白细胞流入和机械性异常性疼痛(以头部退缩力阈值衡量)以及TNFα和IL-1β浓度。在用NK(1)受体拮抗剂SR140333治疗后,也对角叉菜胶诱导的反应进行了评估。向TMJ关节内注射角叉菜胶导致了与机械性异常性疼痛相关的时间依赖性血浆外渗,以及在4至24小时之间明显的中性粒细胞积聚。用SR140333治疗在4小时和24小时时显著抑制了血浆外渗和白细胞流入的增加,以及关节腔内TNFα和IL-1β的产生,但未能影响头部退缩阈值的变化。从目前的TMJ关节炎模型获得的结果首次提供了关于这个实验性炎症过程时间进程的信息。此外,我们的数据表明,外周NK(1)受体介导TMJ中TNFα和IL-1β的产生以及一些炎症体征,如血浆外渗和白细胞流入,但不介导伤害性成分。

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