Amin A R, Abramson S B
Hospital for Joint Diseases, New York, NY 10003, USA.
Curr Opin Rheumatol. 1998 May;10(3):263-8. doi: 10.1097/00002281-199805000-00018.
It is increasingly appreciated that mediators typically associated with inflammatory arthritis, such as catabolic cytokines and nitric oxide, are produced by synovium and cartilage in osteoarthritis. The role that such mediators play in the progression of cartilage degradation in osteoarthritis is under intensive investigation. Nitric oxide is a highly reactive, cytotoxic free radical that has been implicated in tissue injury in a variety of diseases. Cartilage obtained from patients with osteoarthritis produces significant amounts of nitric oxide ex vivo, even in the absence of added stimuli such as interleukin-1 or lipopolysaccharide. In vitro, nitric oxide exerts detrimental effects on chondrocyte functions, including the inhibition of collagen and proteoglycan synthesis, enhanced apoptosis, and an inhibition of B1 integrin-dependent adhesion to the extra-cellular matrix. This paper reviews recent observations regarding the role of nitric oxide in osteoarthritis and presents evidence suggesting that the inhibition of nitric oxide production could be a desirable future therapeutic strategy.
人们越来越认识到，通常与炎性关节炎相关的介质，如分解代谢细胞因子和一氧化氮，是由骨关节炎中的滑膜和软骨产生的。此类介质在骨关节炎软骨降解进展中所起的作用正在深入研究中。一氧化氮是一种高反应性的细胞毒性自由基，与多种疾病的组织损伤有关。即使在没有添加白细胞介素-1或脂多糖等刺激物的情况下，从骨关节炎患者获取的软骨在体外也会产生大量一氧化氮。在体外，一氧化氮对软骨细胞功能产生有害影响，包括抑制胶原蛋白和蛋白聚糖合成、增强细胞凋亡以及抑制β1整合素依赖性细胞与细胞外基质的黏附。本文综述了关于一氧化氮在骨关节炎中作用的近期观察结果，并提供证据表明抑制一氧化氮生成可能是未来一种理想的治疗策略。
