Yaron M, Yaron I, Mashiah V
J Rheumatol. 1984 Aug;11(4):488-92.
Human synovial fibroblasts were "activated" by poly (I) X poly (C) to overproduce prostaglandin E (PGE). Hydrocortisone, diclofenac, indomethacin and ibuprofen inhibited PGE production in a dose dependent manner. Diclofenac (0.2 microgram/ml) had an effect similar to that of 1 microgram/ml of indomethacin and a stronger one than that of 0.5 microgram/ml hydrocortisone and 0.2 microgram/ml ibuprofen. Addition of hydrocortisone with either indomethacin or diclofenac had a synergistic inhibitory effect on PGE production. We suggest that this is an additional model for the study of PGE effect of antirheumatic drugs.
人滑膜成纤维细胞被聚肌苷酸×聚胞苷酸“激活”,从而过量产生前列腺素E(PGE)。氢化可的松、双氯芬酸、吲哚美辛和布洛芬以剂量依赖方式抑制PGE的产生。双氯芬酸(0.2微克/毫升)的作用与1微克/毫升吲哚美辛相似,且比0.5微克/毫升氢化可的松和0.2微克/毫升布洛芬的作用更强。氢化可的松与吲哚美辛或双氯芬酸联合使用对PGE的产生具有协同抑制作用。我们认为这是研究抗风湿药物PGE效应的另一种模型。