McCartney-Francis N, Allen J B, Mizel D E, Albina J E, Xie Q W, Nathan C F, Wahl S M
Laboratory of Immunology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892.
J Exp Med. 1993 Aug 1;178(2):749-54. doi: 10.1084/jem.178.2.749.
Nitric oxide (NO), a toxic radical gas produced during the metabolism of L-arginine by NO synthase (NOS), has been implicated as a mediator of immune and inflammatory responses. A single injection of streptococcal cell wall fragments (SCW) induces the accumulation of inflammatory cells within the synovial tissue and a cell-mediated immune response that leads destructive lesions. We show here that NO production is elevated in the inflamed joints of SCW-treated rats. Administration of NG-monomethyl-L-arginine, an inhibitor of NOS, profoundly reduced the synovial inflammation and tissue damage as measured by an articular index and reflected in the histopathology. These studies implicate the NO pathway in the pathogenesis of an inflammatory arthritis and demonstrate the ability of a NOS inhibitor to modulate the disease.
一氧化氮(NO)是由一氧化氮合酶(NOS)在L-精氨酸代谢过程中产生的一种有毒自由基气体,被认为是免疫和炎症反应的介质。单次注射链球菌细胞壁片段(SCW)可诱导滑膜组织内炎症细胞的积聚以及导致破坏性病变的细胞介导免疫反应。我们在此表明,经SCW处理的大鼠炎症关节中NO的产生增加。给予NOS抑制剂NG-单甲基-L-精氨酸,可显著减轻滑膜炎症和组织损伤,这通过关节指数来衡量,并在组织病理学中得到体现。这些研究表明NO途径参与炎症性关节炎的发病机制,并证明了NOS抑制剂调节该疾病的能力。