Serial determination of tumor necrosis factor-alpha content in rat sciatic nerve after chronic constriction injury
Serial determination of tumor necrosis factor-alpha content in rat sciatic nerve after chronic constriction injury
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DOI：
10.1006/exnr.1999.7193
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发表时间：
1999-11-01
影响因子：
5.3
通讯作者：
Sommer, C
中科院分区：
文献类型：
--
作者：
George, A;Schmidt, C;Sommer, C
周围神经损伤后诱导的沃勒变性与促炎细胞因子的上调相关，促炎细胞因子被认为有助于病变诱导的神经性疼痛的发展。在慢性缩窄性损伤（CCI）（损伤诱导的疼痛性单神经病的动物模型）中，抑制细胞因子肿瘤坏死因子-α（TNF）的合成、释放或功能导致疼痛相关行为减少。本文用酶联免疫法测定了CCI后0、0.5、1、3、7和14天大鼠坐骨神经中TNF含量的变化。在对照神经中已经检测到低水平的TNF。CCI后浓度迅速增加，在12小时达到最大值（2.7倍），并在较低水平上保持升高，直到第3天。在第14天再次达到基线水平。这些结果表明，TNF是在导致周围神经损伤后沃勒变性和痛觉过敏的级联反应中的早期时间点产生的。鉴于只有用TNF抑制剂预防性治疗才能有效降低CCI中的痛觉过敏，TNF似乎有助于该模型中神经性疼痛的起始。(C)北京：科学出版社.
Wallerian degeneration, induced after injury to a peripheral nerve, is associated with, upregulation of proinflammatory cytokines, which are suggested to contribute to the development of lesion-induced neuropathic pain. In chronic constrictive injury (CCI), an animal model of injury-induced painful mononeuropathy, inhibition of synthesis, release, or function of the cytokine tumor necrosis factor-alpha (TNF) results in reduced pain-associated behavior. Here, changes of TNF content in rat sciatic nerves after CCI (days 0, 0.5, 1, 3, 7 and 14) were investigated by enzyme-linked-immunoassay. Low levels of TNF were already detectable in control nerves. Concentrations increased rapidly after CCI, with a maximum (2.7-fold) at 12 h, and remained elevated on a lower level until day 3. Baseline levels were reached again at day 14. These results indicate that TNF is produced at an early time point in the cascade of events resulting in Wallerian degeneration and hyperalgesia following peripheral nerve injury. Given that only prophylactic treatment with TNF inhibitors efficiently reduces hyperalgesia in CCI, TNF seems to contribute to the initiation of neuropathic pain in this model. (C) 1999 Academic Press.