Copelman C A, Diemel L T, Gveric D, Gregson N A, Cuzner M L
Department of Neurochemistry, Institute of Neurology, University College London, 1 Wakefield Street, London, WC1N 1PJ, United Kingdom.
J Neurosci Res. 2001 Dec 15;66(6):1173-8. doi: 10.1002/jnr.10026.
An increased level of myelin basic protein (MBP) degradation peptide 80-89, representative of myelin breakdown, is detected in myelinating foetal rat brain aggregate cultures supplemented with peritoneal macrophages at a time coinciding with the onset of myelination. During the period of myelination, the proportion of activated macrophages/microglia in the aggregates decreases, accompanied by a reduction in the content of MBP degradation products. During the recovery period following a demyelinating episode, the rate of MBP synthesis in antibody-treated standard aggregates was greater than in their medium controls. However, the rate of MBP accumulation was not as efficient in macrophage-enriched aggregates and was associated with persistently raised MBP peptide levels. Thus, as occurs in multiple sclerosis lesions, attempts at remyelination appear to be counterbalanced by macrophage-mediated demyelination, with the continued presence of degraded myelin rendering a local environment that is not fully conducive to remyelination.
在添加腹膜巨噬细胞的髓鞘形成期胎鼠脑聚集培养物中，检测到代表髓鞘分解的髓鞘碱性蛋白（MBP）降解肽80 - 89水平升高，且时间与髓鞘形成开始一致。在髓鞘形成期间，聚集体中活化巨噬细胞/小胶质细胞的比例下降，同时MBP降解产物的含量降低。在脱髓鞘发作后的恢复期，抗体处理的标准聚集体中MBP合成速率高于其培养基对照。然而，富含巨噬细胞的聚集体中MBP积累速率不那么高效，且与MBP肽水平持续升高有关。因此，如同在多发性硬化症病变中发生的那样，再髓鞘化的尝试似乎被巨噬细胞介导的脱髓鞘所抵消，降解髓鞘的持续存在使得局部环境不完全有利于再髓鞘化。
