Kurzepa Jacek, Bartosik-Psujek Halina, Suchozebrska-Jesionek Danuta, Rejdak Konrad, Stryjecka-Zimmer Marta, Stelmasiak Zbigniew
Katedra i Zakład Biochemii, Katedra i Klinika Neurologii, Akademia Medyczna im. prof. Feliksa Skubiszewskiego w Lublinie, ul. Jaczewskiego 8, 20-954 Lublin, Poland.
Neurol Neurochir Pol. 2005 Jan-Feb;39(1):63-7.
Multiple sclerosis (MS) is an autoimmune disease whose features include a massive lymphocyte recruitment into the central nervous system and segmental demyelinization of the white matter. One of the MS development factors is an increase of matrix metalloproteinases (MMPs) activity with a coincidental decrease of tissue inhibitors of MMPs (TIMPs) activity. Investigations of serum, cerebrospinal fluid and brain tissue of patients showed an increase of MMP-1, -2, -3, -7, -9 and MMP-12 activity. MMPs disrupt the blood-brain barrier (BBB), increase lymphocyte migration into the central nervous system and are involved in degradation of myelin proteins. MMPs induce the appearance of an active form of tumor necrosis factor alpha, a strong proinflammatory cytokine. The drugs used in MS treatment decrease MMPs expression. Multiple actions of MMPs prove their involvement in the pathogenesis and treatment of MS.
多发性硬化症（MS）是一种自身免疫性疾病，其特征包括大量淋巴细胞募集进入中枢神经系统以及白质的节段性脱髓鞘。MS发展的因素之一是基质金属蛋白酶（MMPs）活性增加，同时基质金属蛋白酶组织抑制剂（TIMPs）活性降低。对患者血清、脑脊液和脑组织的研究表明，MMP-1、-2、-3、-7、-9和MMP-12活性增加。MMPs破坏血脑屏障（BBB），增加淋巴细胞向中枢神经系统的迁移，并参与髓磷脂蛋白的降解。MMPs诱导肿瘤坏死因子α活性形式的出现，肿瘤坏死因子α是一种强大的促炎细胞因子。用于MS治疗的药物会降低MMPs的表达。MMPs的多种作用证明它们参与了MS的发病机制和治疗。
