Müller H W, Minwegen P
Department of Neurology, University of Düsseldorf, FRG.
J Neurosci Res. 1987;18(1):222-9. doi: 10.1002/jnr.490180132.
The selective toxicity of silica quartz dust to macrophages was used to assess the role of these cells in Wallerian degeneration and nerve repair. Left sciatic nerves of adult Wistar rats were crushed and one group of animals received repetitive intraperitoneal injections of silica (200 mg two times per week starting 1 day prior to injury), whereas the control group received saline. Unexpectedly, silica treatment did not impair the initial invasion of (hematogenous) macrophages into the degenerating distal nerve stump as revealed by histological and immunocytochemical methods. However, 4 weeks after the lesion three specific events in Wallerian degeneration were significantly inhibited in silica-treated animals: 1) inhibition of phagocytosis and degradation of myelin, 2) delay in disappearance of nonresident macrophages from regenerating nerve, 3) reduction of synthesis and/or secretion of apolipoprotein E in resting macrophages. On the other hand, axonal regrowth and remyelination were not affected by silica. These in situ experiments support and extend previous studies suggesting specific functions for nonresident macrophages in Wallerian degeneration of peripheral nerve.
利用二氧化硅石英粉尘对巨噬细胞的选择性毒性来评估这些细胞在沃勒变性和神经修复中的作用。将成年Wistar大鼠的左侧坐骨神经压伤，一组动物从损伤前1天开始每周两次腹腔注射二氧化硅（200毫克），而对照组注射生理盐水。出乎意料的是，组织学和免疫细胞化学方法显示，二氧化硅处理并未损害（血源性）巨噬细胞对变性远端神经残端的初始侵入。然而，损伤后4周，二氧化硅处理的动物中沃勒变性的三个特定事件受到显著抑制：1）吞噬作用和髓磷脂降解的抑制；2）再生神经中非驻留巨噬细胞消失延迟；3）静息巨噬细胞中载脂蛋白E合成和/或分泌减少。另一方面，轴突再生和髓鞘再生不受二氧化硅影响。这些原位实验支持并扩展了先前的研究，表明非驻留巨噬细胞在周围神经沃勒变性中具有特定功能。
