Amin A R, Attur M, Abramson S B
Department of Rheumatology and Medicine, Hospital for Joint Diseases, NYU School of Medicine, New York, New York 10003, USA.
Curr Opin Rheumatol. 1999 May;11(3):202-9. doi: 10.1097/00002281-199905000-00009.
Nitric oxide (NO) and prostaglandin E2 (PGE2) are two pleiotropic inflammatory mediators overproduced in arthritis-affected joints. The inducible isoform of nitric oxide synthase (iNOS) and cyclooxygenase (COX-2) are found both in the synovial tissue and in the cartilage. Their expression is regulated by catabolic cytokines, such as interleukin-1beta and tumor necrosis factor-alpha. These inflammatory mediators play a profound role in the pathogenic processes that arise in the pannus of rheumatoid arthritis and also interfere with cartilage homeostasis in osteoarthritis. Several drugs, including nonsteroidal anti-inflammatory drugs, immunosuppressive agents, and tetracyclines, attenuate the activity of NO and PGE2. These pleiotropic mediators are targets for pharmacologic intervention and gene therapy.
一氧化氮（NO）和前列腺素E2（PGE2）是在关节炎受累关节中过度产生的两种多效性炎症介质。一氧化氮合酶（iNOS）和环氧化酶（COX-2）的诱导型同工型在滑膜组织和软骨中均有发现。它们的表达受分解代谢细胞因子如白细胞介素-1β和肿瘤坏死因子-α的调节。这些炎症介质在类风湿关节炎血管翳中出现的致病过程中起重要作用，并且也干扰骨关节炎中的软骨稳态。包括非甾体抗炎药、免疫抑制剂和四环素在内的几种药物可减弱NO和PGE2的活性。这些多效性介质是药物干预和基因治疗的靶点。
