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Abstract
Gold compounds are widely used in the treatment of rheumatoid arthritis, but their mechanisms of action remain unclear. We demonstrate here that auranofin (AF) (0.1-3 microM), but neither the hydrophilic gold compounds aurothiomalate (ATM) and aurothioglucose nor methotrexate or D-penicillamine, inhibits the induction of interleukin 1 beta and tumor necrosis factor (TNF) alpha mRNA and protein by either zymosan, lipopolysaccharide (LPS), or various bacteria in mouse macrophages. The auranofin-mediated inhibition of the induction of TNF-alpha mRNA was stronger than that of interleukin (IL) 1 beta mRNA. AF, but not the other drugs, also inhibited zymosan-induced mobilization of arachidonate. The fact that AF inhibited the induction of mRNA for both these proinflammatory cytokines, irrespective of which stimulus was used, may indicate that it affects some common signal transduction step vital to their induction.
| Original language | English |
|---|---|
| Pages (from-to) | 1753-9 |
| Journal | Biochemical Pharmacology |
| Volume | 50 |
| Issue number | 11 |
| Publication status | Published - 1995 |
Subject classification (UKÄ)
- Basic Medicine
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Dive into the research topics of 'Auranofin inhibits the induction of interleukin 1beta and tumor necrosis factor alpha mRNA in macrophages'. Together they form a unique fingerprint.Research output
- 1 Doctoral Thesis (compilation)
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Effects of disease-modifying antirheumatic drugs on macrophage signal transduction and the induction of proinflammatory cytokines
Bondeson, J., 1996, Department of Cell and Molecular Biology, Lund University. 190 p.Research output: Thesis › Doctoral Thesis (compilation)