骨关节炎和类风湿性关节炎软骨中一氧化氮生成的调节。内源性白细胞介素-1抑制剂的作用。
Regulation of nitric oxide production in osteoarthritic and rheumatoid cartilage. Role of endogenous IL-1 inhibitors.
作者信息
Vuolteenaho Katriina, Moilanen Taemu, Hämäläinen Mari, Moilanen Eeve
机构信息
The Immunopharmacological Research Group, Medical School, University of Tampere, and Tampere University Hospital, Finland.
出版信息
Scand J Rheumatol. 2003;32(1):19-24. doi: 10.1080/03009740310000355.
OBJECTIVE
To investigate the endogenous regulation of interleukin-1 (IL-1) cytokine network in osteoarthritic (OA) and rheumatoid (RA) cartilage in relation to nitric oxide (NO) production.
METHODS
Cartilage specimen obtained from OA and RA patients undergoing knee replacement surgery were studied for iNOS expression, NO and IL-1 antagonist production in tissue culture.
RESULTS
OA cartilage responded to IL-1beta-stimulation with higher NO production than RA cartilage, whereas there was no difference in NO synthesis between OA and RA samples when stimulated by TNFalpha or LPS. Interleukin-1 receptor antagonist (IL-1Ra) production was higher in RA cartilage than in OA cartilage, and its production was increased by NO synthase inhibitor 1400W.
CONCLUSION
IL-1beta is a potent stimulator of NO production by the iNOS pathway in RA and more pronouncedly in OA cartilage. This process is regulated by cartilage derived IL-1 antagonists, and is implicated in cartilage destruction and synovial inflammation in OA and RA joints.
目的
研究骨关节炎（OA）和类风湿关节炎（RA）软骨中白细胞介素-1（IL-1）细胞因子网络与一氧化氮（NO）产生相关的内源性调节。
方法
对接受膝关节置换手术的OA和RA患者的软骨标本进行研究，检测组织培养中诱导型一氧化氮合酶（iNOS）表达、NO和IL-1拮抗剂的产生情况。
结果
与RA软骨相比，OA软骨对IL-1β刺激产生的NO更多，而当受到肿瘤坏死因子α（TNFα）或脂多糖（LPS）刺激时，OA和RA样本之间的NO合成没有差异。RA软骨中白细胞介素-1受体拮抗剂（IL-1Ra）的产生高于OA软骨，且其产生可被NO合酶抑制剂1400W增加。
结论
IL-1β是RA中通过iNOS途径产生NO的有效刺激物，在OA软骨中更明显。这一过程受软骨来源的IL-1拮抗剂调节，与OA和RA关节中的软骨破坏和滑膜炎症有关。
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