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首页> 外文期刊>CNS drug reviews >Glatiramer acetate in multiple sclerosis: a review.
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Glatiramer acetate in multiple sclerosis: a review.

机译：醋酸格拉替雷在多发性硬化症中的研究进展。

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Multiple sclerosis (MS) is considered to be primarily an inflammatory autoimmune disease. Over the last 5 years, our view of the pathogenesis of MS has evolved considerably. The axonal damage was recognized as an early event in the disease process and as an important determinant of long-term disability. Therefore, the antiinflammatory and neuroprotective strategies are thought to represent promising approach to the therapy of MS. The therapeutic potential of glatiramer acetate (GA), a synthetic amino acid polymer composed of a mixture of L-glutamic acid, L-lysine, L-alanine, and L-tyrosine in defined proportions, in MS has been apparent for many years. GA has been shown to be effective in preventing and suppressing experimental allergic encephalomyelitis (EAE), the animal model of MS. GA has been, therefore, evaluated in several clinical studies and found to alter the natural history of relapsing-remitting (RR)MS by reducing the relapse rate and affecting disability. These findings were confirmed in open-label follow-up trials covering more than 10 years of treatment. The trials demonstrated sustained efficacy for GA in slowing the progression of disability. The clinical therapeutic effect of GA is consistent with the results of magnetic resonance imaging (MRI) findings from various clinical centers. At a daily standard dose of 20 mg, s.c., GA was generally well tolerated. The induction of GA-reactive T-helper 2-like regulatory suppressor cells is thought to be the main mechanism of the therapeutic action of this drug. In addition, it was recently shown that GA-reactive T cells produce neurotrophic factors (e.g., brain-derived neurotrophic factor [BDNF]) that protect neurons and axons in the area of injury.
机译：多发性硬化症（MS）被认为主要是一种炎症性自身免疫性疾病。在过去的5年中，我们对MS发病机理的看法已发生了很大变化。轴突损伤被认为是疾病过程中的早期事件，是长期残疾的重要决定因素。因此，抗炎和神经保护策略被认为是治疗MS的有前途的方法。醋酸格拉替雷（GA）是一种合成氨基酸聚合物，由L-谷氨酸，L-赖氨酸，L-丙氨酸和L-酪氨酸按规定比例组成，在MS中的治疗潜力已显现多年。已经证明GA可以有效预防和抑制MS的动物模型实验性变应性脑脊髓炎（EAE）。因此，GA已在多项临床研究中进行了评估，并发现GA通过降低复发率和影响残疾来改变复发-缓解（RR）MS的自然史。这些发现在涵盖10多年治疗的开放性随访试验中得到了证实。这些试验证明了GA在减缓残疾发展方面具有持续的功效。 GA的临床治疗效果与来自各个临床中心的磁共振成像（MRI）结果一致。在每日标准剂量为20 mg s.c.的情况下，GA一般耐受良好。认为GA反应性T辅助2样调节性抑制细胞的诱导是该药物治疗作用的主要机制。另外，最近显示GA反应性T细胞产生神经营养因子（例如脑源性神经营养因子[BDNF]），其在损伤区域保护神经元和轴突。

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