Jean Isabelle, Allamargot Chantal, Barthelaix-Pouplard Annick, Fressinaud Catherine
Cell Biology Laboratory, UPRES EA 3143, University Hospital, 4 rue Larrey, F 49033 Angers Cedex, France.
Neuroreport. 2002 Apr 16;13(5):627-31. doi: 10.1097/00001756-200204160-00018.
In multiple sclerosis (MS), demyelination is often accompanied by axonal lesions, which largely account for patient disability. We therefore studied the consequences of demyelination induced by lysophosphatidylcholine (LPC) on the axonal cytoskeleton, particularly neurofilaments (NF) and tubulin, in the adult rat corpus callosum. Immunocytochemistry showed that NF immunolabelled fibres decreased by 49% in the LPC injured area at day 15. Since it has been previously demonstrated that PDGF improves remyelination, we performed a comparative study between LPC controls and PDGF-treated (1 microg) animals. In these later animals, immunolabelling for NFL and NFM (NFH subunit excepted) was increased by 142 and 63%, respectively, indicating reduction of axonal abnormalities. These results extend the potential therapeutic role of PDGF in MS.
在多发性硬化症（MS）中，脱髓鞘通常伴有轴突损伤，这在很大程度上导致了患者的残疾。因此，我们研究了溶血磷脂酰胆碱（LPC）诱导的脱髓鞘对成年大鼠胼胝体轴突细胞骨架的影响，特别是神经丝（NF）和微管蛋白。免疫细胞化学显示，在第15天，LPC损伤区域的NF免疫标记纤维减少了49%。由于先前已证明血小板衍生生长因子（PDGF）可改善髓鞘再生，我们对LPC对照组和经PDGF治疗（1微克）的动物进行了一项比较研究。在这些后期动物中，NFL和NFM（除NFH亚基外）的免疫标记分别增加了142%和63%，表明轴突异常减少。这些结果扩展了PDGF在MS中的潜在治疗作用。
