Yong V Wee
Hotchkiss Brain Institute and Department of Clinical Neuroscience, University of Calgary, Calgary, Canada.
J Neurol Sci. 2009 Feb 1;277 Suppl 1:S16-8. doi: 10.1016/S0022-510X(09)70006-1.
In multiple sclerosis, physiological repair mechanisms can help the nervous system to recover from tissue injury. Enhancing such repair mechanisms is an important, and increasingly realistic, therapeutic goal in multiple sclerosis. With respect to remyelination, several promising therapeutic avenues are currently being explored, including stem cell transplantation, LINGO-1, prolactin and glatiramer acetate. Glatiramer acetate is believed to act by the induction of specific populations of anti-inflammatory Th2 cells or Type 2 monocytes which infiltrate sites of injury in the nervous system where they release anti-inflammatory cytokines leading to bystander suppression of inflammation. In addition, these cells can release neurotrophic factors such as BDNF and IGF-1 which have been shown to stimulate the differentiation of oligodendrocyte precursor cells and thus enhance remyelination. In addition, neurotrophic factors released in response to glatiramer acetate may stimulate the differentiation of neuronal progenitor cells into mature neurones that can replace neurones lost through the disease process. This repair capacity of glatiramer acetate may contribute to the long-term well-being of patients with multiple sclerosis treated with glatiramer acetate.
在多发性硬化症中，生理修复机制有助于神经系统从组织损伤中恢复。增强这种修复机制是多发性硬化症中一个重要且越来越可行的治疗目标。关于髓鞘再生，目前正在探索几种有前景的治疗途径，包括干细胞移植、LINGO - 1、催乳素和醋酸格拉替雷。据信醋酸格拉替雷的作用机制是诱导特定群体的抗炎性Th2细胞或2型单核细胞，这些细胞浸润神经系统的损伤部位，在那里它们释放抗炎细胞因子，从而导致旁观者对炎症的抑制。此外，这些细胞可以释放神经营养因子，如脑源性神经营养因子（BDNF）和胰岛素样生长因子 - 1（IGF - 1），已证明这些因子可刺激少突胶质细胞前体细胞的分化，从而增强髓鞘再生。此外，对醋酸格拉替雷产生反应而释放的神经营养因子可能刺激神经元祖细胞分化为成熟神经元，这些成熟神经元可以替代在疾病过程中丢失的神经元。醋酸格拉替雷的这种修复能力可能有助于接受醋酸格拉替雷治疗的多发性硬化症患者的长期健康。
