DICLOFENAC INHIBITS MONOCYTE SUPEROXIDE PRODUCTION EXVIVO IN RHEUMATOID-ARTHRITIS

被引：15

作者：

BELL, AL

ADAMSON, H

KIRK, F

MCCAIGUE, MD

ROTMAN, H

机构：

[1] QUEENS UNIV BELFAST,DEPT MED,BELFAST BT7 1NN,ANTRIM,NORTH IRELAND

[2] CIBA GEIGY PHARMACEUT CORP,HORSHAM,W SUSSEX,ENGLAND

来源：

RHEUMATOLOGY INTERNATIONAL | 1991年 / 11卷 / 01期

关键词：

MONOCYTE; SUPEROXIDE; RHEUMATOID ARTHRITIS; DICLOFENAC; ANTIINFLAMMATORY DRUG;

D O I：

10.1007/BF00290247

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Effects of the nonsteroidal anti-inflammatory drug, diclofenac, on stimulated monocyte superoxide production were assessed directly in vitro and following treatment of patients with rheumatoid arthritis ex vivo. Diclofenac inhibited superoxide generation provoked by serum treated symosan (STZ) and fluoride anion (F) but not by phorbol myristate acetate (PMA) in vitro. Following patient therapy, inhibition of superoxide production occurred when STZ and PMA, but not F were used as stimuli. No changes were seen in control subjects. The contrasting profiles of inhibition seen in vitro and ex vivo suggest an indirect effect on superoxide production during clinical use of the agent. These data are consistent with the hypothesis that anti-inflammatory drugs may act in rheumatoid arthritis by inhibiting phagocyte superoxide anion production.

引用

页码：27 / 30

页数：4

共 18 条

[1]

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