Tumour necrosis factor-α and apoptosis in the rat temporomandibular joint

Tumour necrosis factor-α and apoptosis in the rat temporomandibular joint
复制标题

DOI:
10.1016/s0003-9969(03)00175-4
复制
发表时间:
2003-12-01
影响因子:
3
通讯作者:
Hutchins, B
Hutchins, B
中科院分区:
医学4区
文献类型:
--
作者:
Spears, R;Oakes, R;Hutchins, B

文献摘要

被引文献

相似文献

本研究的目的是探讨肿瘤坏死因子-α (TNF-α) 和细胞凋亡在颞下颌关节 (TMJ) 急性炎症过程中的作用。将成年雄性斯普拉格-道利大鼠的颞下颌关节注射完全弗氏佐剂(CFA),或将其作为未注射的对照。注射后 2 天取出 TMJ 组织以模拟急性炎症条件,并分析 TNF-α、受体 TNF-R1、caspase-3 和 -8 表达以及细胞凋亡的变化。与未注射的对照相比,注射 CFA 的动物中 TNF-α、TNF-R1、caspase-3 和 -8 的浓度以及细胞凋亡显着升高。组织与 TNF-α 孵育导致 caspase-3 和 -8 显着增加。此外,炎症期间细胞凋亡水平显着增加,这可以通过添加抗 TNF-α 中和抗体或半胱天冬酶抑制剂来抑制。 TNF-α可能在CFA诱导的急性颞下颌关节炎症的发生中发挥重要作用,并且可能涉及细胞凋亡信号通路的激活。 (C) 2003 Elsevier Ltd. 所有,保留权利。
The purpose of this investigation was to investigate the roles that tumour necrosis factor-alpha (TNF-alpha) and apoptosis play during acute inflammation of the temporomandibular joint (TMJ). Adult mate Sprague-Dawley rats were injected with complete Freund's adjuvant (CFA) into the TMJ or kept as uninjected controls. The TMJ tissues were removed 2 days post-injection to mimic conditions of acute inflammation and analysed for changes in expression of TNF-alpha, the receptor TNF-R1, caspase-3 and -8, and apoptosis. Concentrations of TNF-alpha, TNF-R1, caspase-3 and -8, and apoptosis were significantly elevated in CFA-injected animals compared to uninjected controls. Tissue incubation with TNF-alpha caused a significant increase in caspase-3 and -8. Also, levels of apoptosis were significantly increased during inflammation, which could be inhibited by the addition of either anti-TNF-alpha neutralising antibody or caspase inhibitors. TNF-alpha may play a significant role in the onset of acute CFA-induced TMJ inflammation, and activation of apoptosis signalling pathways may be involved. (C) 2003 Elsevier Ltd. All, rights reserved.