Vuolteenaho K, Moilanen T, Knowles R G, Moilanen E
The Immunopharmacology Research Group, Medical School, University of Tampere and Research Unit, Tampere University Hospital, Tampere, Finland.
Scand J Rheumatol. 2007 Jul-Aug;36(4):247-58. doi: 10.1080/03009740701483014.
Elevated levels of markers of nitric oxide (NO) production are found in osteoarthritic joints suggesting that NO is involved in the pathogenesis of osteoarthritis (OA). In OA, NO mediates many of the destructive effects of interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha) in the cartilage, and inhibitors of NO synthesis have demonstrated retardation of clinical and histological signs and symptoms in experimentally induced OA and other forms of arthritis. As an important factor in cartilage, the regulation of inducible nitric oxide synthase (iNOS) expression and activity, and the effects of NO are reviewed, especially in relation to the pathogenesis of OA.
在骨关节炎关节中发现一氧化氮（NO）生成标志物水平升高，这表明NO参与了骨关节炎（OA）的发病机制。在OA中，NO介导了白细胞介素-1（IL-1）和肿瘤坏死因子-α（TNF-α）对软骨的许多破坏作用，并且NO合成抑制剂已证明可延缓实验性诱导的OA和其他形式关节炎的临床及组织学体征和症状。作为软骨中的一个重要因素，本文综述了诱导型一氧化氮合酶（iNOS）表达和活性的调节以及NO的作用，特别是与OA发病机制相关的方面。
