Caltabiano M M, Koestler T P, Poste G, Greig R G
Biochem Biophys Res Commun. 1986 Aug 14;138(3):1074-80. doi: 10.1016/s0006-291x(86)80391-6.
In vitro exposure of cultured human, murine and rat cells to pharmacologic concentrations (10(-8) to 10(-6) M) of auranofin, 2,3,4,6,-tetra-O-acetyl-1-thio-beta-D-glucopyranosato-S- triethylphosphine gold(I) (Ridaura), a gold containing compound approved for the treatment of rheumatoid arthritis, results in the induction of several stress proteins. The enhanced synthesis of two polypeptides, p32 and p34, was particularly prominent. A similar response was observed in freshly collected human monocytes challenged with auranofin. In addition, oral administration of auranofin to rats induced enhanced synthesis of a 32-kDa protein in peritoneal exudate cells analyzed ex vivo at various times following drug treatment. These data suggest that increased synthesis of p32 and p34 might participate in mediating certain aspects of auranofin pharmacology.
将培养的人、小鼠和大鼠细胞在体外暴露于金诺芬（瑞得，2,3,4,6-四-O-乙酰基-1-硫代-β-D-吡喃葡萄糖基-S-三乙膦金(I)）的药理浓度（10⁻⁸至10⁻⁶M），该含金化合物被批准用于治疗类风湿性关节炎，结果会诱导几种应激蛋白的产生。两种多肽p32和p34的合成增强尤为显著。在用金诺芬刺激的新鲜采集的人单核细胞中也观察到类似反应。此外，给大鼠口服金诺芬后，在药物治疗后的不同时间对腹腔渗出细胞进行离体分析，发现一种32 kDa蛋白的合成增强。这些数据表明，p32和p34合成增加可能参与介导金诺芬药理学的某些方面。
