Nitric oxide synthase and cyclooxygenases: Distribution, regulation, and intervention in arthritis
Nitric oxide synthase and cyclooxygenases: Distribution, regulation, and intervention in arthritis
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DOI：
10.1097/00002281-199905000-00009
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发表时间：
1999-05-01
影响因子：
5.1
通讯作者：
Abramson, Steven B.
中科院分区：
文献类型：
--
作者：
Amin, Ashok R.;Attur, Mukundan;Abramson, Steven B.
一氧化氮（NO）和前列腺素E2 （PGE2）是两种在关节炎影响的关节中过量产生的多效炎症介质。一氧化氮合酶（iNOS）和环氧合酶（COX-2）的诱导异构体存在于滑膜组织和软骨中。它们的表达受分解代谢细胞因子，如白细胞介素-1和肿瘤坏死因子-调节。这些炎症介质在类风湿关节炎的发病过程中发挥着重要作用，也干扰骨关节炎的软骨稳态。几种药物，包括非甾体抗炎药、免疫抑制剂和四环素，可减弱NO和PGE2的活性。这些多效介质是药物干预和基因治疗的靶点。
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-1 [beta] 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.