Winther K, Oxholm P, Sengeløv H
Department of Clinical Chemistry, Medical Department TTA, Rigshospitalet, Copenhagen, Denmark.
Inflammation. 1988 Feb;12(1):107-12. doi: 10.1007/BF00915896.
Auranofin (Aur), a new oral gold compound valuable in treatment of patients with rheumatoid arthritis, is known to have an inhibitory effect on ADP- and epinephrine-induced platelet aggregation in vitro. This may be of clinical importance as platelets participate in thrombus formation and are believed to act as proinflammatory cells in the diseased synovial tissue of rheumatoid arthritis. In the present in vitro study it was confirmed that Aur inhibits both ADP- and adrenaline-induced platelet aggregation in a dose- and time-dependent manner. In addition, a time- and dose-dependent decrease in platelet release of serotonin as well as a pronounced increase in the production of cyclic-AMP was found to result from Aur incubation. Aur's inhibitory effect on platelets is probably mediated through cyclic-AMP stimulation. Future studies of Aur's platelet inhibitory effect should investigate the mechanisms by which cyclic-AMP formation is increased, since this may be of importance also for Aur's action on other cell types.
金诺芬（Aur）是一种对类风湿关节炎患者治疗有价值的新型口服金化合物，已知其在体外对ADP和肾上腺素诱导的血小板聚集有抑制作用。这可能具有临床重要性，因为血小板参与血栓形成，并且被认为在类风湿关节炎患病滑膜组织中作为促炎细胞起作用。在本体外研究中，证实金诺芬以剂量和时间依赖性方式抑制ADP和肾上腺素诱导的血小板聚集。此外，发现金诺芬孵育导致血清素的血小板释放呈时间和剂量依赖性降低以及环磷酸腺苷的产生明显增加。金诺芬对血小板的抑制作用可能是通过刺激环磷酸腺苷介导的。关于金诺芬血小板抑制作用的未来研究应调查环磷酸腺苷形成增加的机制，因为这可能对金诺芬对其他细胞类型的作用也很重要。
