RT期刊文章SR电子T1基质金属蛋白酶在慢性炎性脱髓鞘upregulation多神经病,使得非vasculitic神经病摩根富林明神经学神经学乔FD Lippincott Williams &威尔金斯SP 62 OP 62做10.1212 / WNL.53.1.62 VO 53是1 A1 d Leppert A1 p·休斯A1 A1 首页b .白尾海雕A1 c . s . Huber Grygar A1 g . A1 K.M.米勒A1 A.J. Steck A1说。Probst A1 p·富尔年1999 UL http://n.neurol首页ogy.org/content/53/1/62.abstract AB目的:确定基质金属蛋白酶的表达模式和细胞来源基质金属蛋白酶在慢性炎性脱髓鞘多神经病(CIDP),使得非vasculitic神经病变(NSVN)。背景:基质金属蛋白酶是肽链内切酶参与免疫细胞组织破坏和渗透的多发性硬化症和格林-巴利综合征。基质金属蛋白酶的酶抑制剂减弱相应临床症状在这些疾病的动物模型。因此MMP的抑制可能是一个新颖的方法治疗CIDP NSVN。然而,基质金属蛋白酶表达谱的慢性炎性疾病尚未建立。方法:MMP-2的表达、MMP-3 MMP-7, MMP-9 T细胞,巨噬细胞,并在CIDP基质细胞,检测不到发炎NSVN,迹象神经病变(外祖母)是通过免疫组织化学方法测定的数量。结果与临床和电生理学的研究结果。结果:生产MMP-2 MMP-9增加在CIDP的神经组织和NSVN而外祖母。T细胞是MMP-2的主要来源和MMP-9 CIDP NSVN,而巨噬细胞只有一个小程度上作出贡献。 Stromal cells of the perineurium/epineurium are an additional source of MMP-2 in NSVN, but not in CIDP. Expression of MMP-3 and MMP-7 was not detectable in CIDP or NSVN. Expression of MMP-2 and MMP-9 did not correlate with clinical disease activity and electrophysiologic measurements. Conclusions: The upregulation of MMP-2 and MMP-9 is a specific feature of CIDP and NSVN, and selective inhibitors of these enzymes could be used to prevent inflammatory tissue damage. The similar increase of MMP-2 and MMP-9 in both demyelinating (CIDP) and nondemyelinating (NSVN) neuropathies raises doubts about whether MMPs play a primary role in demyelination.

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