George Annette, Buehl Achim, Sommer Claudia
Neurologische Klinik der Universität Würzburg, Würzburg, Germany.
Neurosci Lett. 2004 Dec 6;372(3):215-9. doi: 10.1016/j.neulet.2004.09.075.
The pro-inflammatory cytokine tumor necrosis factor-alpha (TNF) contributes to injury-induced peripheral nerve pathology and to the development of neuropathic pain. Here, we investigated whether TNF protein is altered at the site of crush injury of rat sciatic nerve using enzyme-linked immunoassay (ELISA) and immunohistochemistry (IHC). TNF protein levels determined by ELISA were low in nerve homogenates from naive rats. After crush injury, local TNF increased rapidly with a two-fold increase on day 0.5. TNF content remained elevated on day 3 and returned to baseline levels again by day 14 after crush. IHC revealed prominent TNF-immunoreactivity in many epineurial macrophages on days 0.5 to 3 after crush injury. These data indicate that TNF protein is early and transiently upregulated at the site of peripheral nerve trauma.
促炎细胞因子肿瘤坏死因子-α(TNF)会导致损伤诱导的外周神经病理变化以及神经性疼痛的发展。在此,我们使用酶联免疫吸附测定(ELISA)和免疫组织化学(IHC)研究了大鼠坐骨神经挤压伤部位的TNF蛋白是否发生改变。通过ELISA测定,未受伤大鼠神经匀浆中的TNF蛋白水平较低。挤压伤后,局部TNF迅速增加,在第0.5天增加了两倍。TNF含量在第3天仍保持升高,并在挤压伤后第14天再次恢复到基线水平。免疫组织化学显示,挤压伤后第0.5至3天,许多神经外膜巨噬细胞中有明显的TNF免疫反应性。这些数据表明,TNF蛋白在外周神经创伤部位早期且短暂地上调。