Remvig L, Andersen B
Department of Medicine TTA, Rigshospitalet, University of Copenhagen, Denmark.
Scand J Rheumatol. 1990;19(1):11-6. doi: 10.3109/03009749009092617.
Monocytes (M phi) were simultaneously preincubated with salicylazosulfapyridine (Salazopyrin) (SAZ), 0.78-12.5 mM, and lipopolysaccharide from E. coli, 1 X 10(-9) g/ml. Presence of SAZ resulted in a dose-dependent decrease in the co-stimulatory activity in M phi culture supernatants, corresponding to a 50% reduction by SAZ, 2.0 mM. Co-stimulatory activity was estimated by the mitogen-induced thymocyte proliferation assay (THY assay). The results indicate an inhibitory effect of SAZ in vitro on the production of IL-1 and other possible co-stimulatory factors. This inhibitory effect was not due to decreased M phi viability, production of suppressive substances, or to drug interference with the THY assay. Equimolar preincubations with sulfapyridine, 5-aminosalicylic acid and N-acety-1-5-aminosalicylic acid were without effect on the production of co-stimulatory factors.
将单核细胞(M phi)与柳氮磺吡啶(Salazopyrin)(SAZ)(0.78 - 12.5 mM)和来自大肠杆菌的脂多糖(1×10⁻⁹ g/ml)同时进行预孵育。SAZ的存在导致M phi培养上清液中的共刺激活性呈剂量依赖性降低,SAZ浓度为2.0 mM时共刺激活性降低了50%。通过丝裂原诱导的胸腺细胞增殖试验(THY试验)评估共刺激活性。结果表明SAZ在体外对IL - 1和其他可能的共刺激因子的产生具有抑制作用。这种抑制作用并非由于M phi活力降低、抑制性物质的产生或药物对THY试验的干扰所致。用磺胺吡啶、5 - 氨基水杨酸和N - 乙酰 - 1 - 5 - 氨基水杨酸进行等摩尔预孵育对共刺激因子的产生没有影响。