Prosiegel M, Neu I, Vogl S, Hoffmann G, Wildfeuer A, Ruhenstroth-Bauer G
Department of Neurology, Fachklinik Enzensberg, Hopfen am See, West Germany.
Acta Neurol Scand. 1990 Mar;81(3):237-8. doi: 10.1111/j.1600-0404.1990.tb00973.x.
It has recently been suggested that the sulfidopeptide leukotriene C4 (LTC4), a 5-lipoxygenase product of the arachidonic acid metabolism and one of the most potent mediators of vascular permeability, might be involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS). Subsequently, 20 guinea pigs with EAE were treated with sulfasalazine, a substance with a proved leukotriene inhibiting effect, which has previously been described as exerting beneficial effects in patients with inflammatory bowel disease and rheumatoid arthritis. The sulfasalazine-treated guinea pigs showed a significantly better clinical outcome, as well as a significantly lower histological inflammation score compared with 19 controls.
最近有人提出，硫肽白三烯C4（LTC4），作为花生四烯酸代谢的5-脂氧合酶产物以及血管通透性最强的介质之一，可能参与了实验性自身免疫性脑脊髓炎（EAE）和多发性硬化症（MS）的发病机制。随后，对20只患有EAE的豚鼠用柳氮磺胺吡啶进行治疗，柳氮磺胺吡啶是一种已证实具有白三烯抑制作用的物质，此前已被描述为对炎症性肠病和类风湿性关节炎患者有有益作用。与19只对照组相比，接受柳氮磺胺吡啶治疗的豚鼠临床结果明显更好，组织学炎症评分也显著更低。
