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类风湿性滑膜炎中类花生酸的产生。

Eicosanoid production in rheumatoid synovitis.

作者信息

Moilanen E, Alanko J, Nissilä M, Hämäläinen M, Isomäki H, Vapaatalo H

机构信息

Department of Biomedical Sciences, University of Tampere, Finland.

出版信息

Agents Actions. 1989 Nov;28(3-4):290-7. doi: 10.1007/BF01967417.

Abstract

Leukotriene B4 (LTB4) synthesis in rheumatoid synovitis was studied using peripheral and synovial fluid polymorphonuclear leukocytes (PMNs) and rheumatic synovial lining cells. No differences were found in LTB4 synthesis between peripheral PMNs from healthy volunteers and rheumatoid arthritis patients. When peripheral and synovial PMNs from the same RA patient were compared, arachidonic acid-induced LTB4 synthesis in synovial fluid PMNs was increased 1.7-7.2 fold, whereas the response to Ca ionophore A23187 stimulation was similar. This suggests 5-lipoxygenase stimulating factor(s) in inflamed joints. Rheumatic synovial lining cells in a primary cell culture produced small amounts of LTB4, the concentrations being less than 0.1 per cent of those of prostaglandin E2 (PGE2). PGE2 synthesis in synovial cells was increased when arachidonic acid or interleukin-1 was added to the culture, whereas LTB4 production remained unaltered. The present results suggest that in inflamed joints LTB4 originates mainly from PMNs whereas synovial lining cells are the source for PGE2.

摘要

利用外周血和滑液中的多形核白细胞(PMN)以及风湿性滑膜衬里细胞,对类风湿性滑膜炎中白三烯B4(LTB4)的合成进行了研究。健康志愿者和类风湿性关节炎患者外周血PMN的LTB4合成未发现差异。当比较同一类风湿性关节炎患者的外周血和滑膜PMN时,花生四烯酸诱导的滑液PMN中LTB4合成增加了1.7至7.2倍,而对钙离子载体A23187刺激的反应相似。这表明炎症关节中存在5-脂氧合酶刺激因子。原代细胞培养中的风湿性滑膜衬里细胞产生少量LTB4,其浓度低于前列腺素E2(PGE2)浓度的0.1%。当向培养物中添加花生四烯酸或白细胞介素-1时,滑膜细胞中PGE2的合成增加,而LTB4的产生保持不变。目前的结果表明,在炎症关节中,LTB4主要来源于PMN,而滑膜衬里细胞是PGE2的来源。

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