Bondeson J, Sundler R
Department of Cell and Molecular Biology, Lund University, Sweden.
Biochem Pharmacol. 1995 Nov 27;50(11):1753-9. doi: 10.1016/0006-2952(95)02030-6.
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.
金化合物被广泛用于治疗类风湿性关节炎，但其作用机制仍不清楚。我们在此证明，金诺芬（AF）（0.1 - 3微摩尔），而非亲水性金化合物硫代苹果酸金钠（ATM）和硫代葡萄糖金，也非甲氨蝶呤或D - 青霉胺，可抑制酵母聚糖、脂多糖（LPS）或各种细菌在小鼠巨噬细胞中诱导白细胞介素1β和肿瘤坏死因子（TNF）α的mRNA及蛋白表达。金诺芬介导的对TNF - α mRNA诱导的抑制作用强于白细胞介素（IL）1β mRNA。AF而非其他药物，也抑制酵母聚糖诱导的花生四烯酸动员。AF抑制这两种促炎细胞因子mRNA的诱导，无论使用何种刺激，这一事实可能表明它影响了对其诱导至关重要的一些共同信号转导步骤。
