Hernvann A, Bourely B, Le Maire V, Aussel C, Menkes C J, Ekindjian O G
Laboratoire de Biochimie Cellulaire de l'Inflammation, Université Paris XI, Chatenay-Malabry, France.
Eur J Pharmacol. 1996 Oct 24;314(1-2):193-6. doi: 10.1016/s0014-2999(96)00541-9.
Synovial cell cultures prepared from samples taken from osteoarthritic and rheumatoid patients were treated with different anti-inflammatory agents (cortisol, indomethacin, ibuprofen and piroxicam) to determine their 'anti-interleukin-1 beta' action, using inhibition of interleukin-1 beta-mediated glucose uptake stimulation as a biological test. Confluent cells were treated for 24 h with different concentrations of these drugs (10(-5), 10(-6) and 10(-7) mol/l) to study their effect on the inflammation process. 6 h before glucose uptake studies, interleukin-1 beta (1 ng/ml) was added. Whereas non-steroid anti-inflammatory agents were inefficient, cortisol inhibited the action of interleukin-1 beta on glucose uptake. In osteoarthritic cells, cortisol, 10(-5) mol/l, reduced interleukin-1 beta-mediated glucose uptake by 27% after a 24-h incubation. In rheumatoid cells, stimulated 2-deoxy-D-glucose uptake was reduced by 40.6%. Results were similar when interleukin-1 beta and cortisol were added simultaneously, 6 h before glucose uptake was measured. This rapid effect of cortisol was protein synthesis-dependent (inhibited by cycloheximide). Cortisol decreased glucose uptake by synoviocytes by acting on basal and interleukin-1 beta-mediated glucose uptake. This effect was more pronounced in rheumatoid synovial cells. The inhibition of interleukin-1 beta-mediated glucose uptake could be proposed as a new model for studying the anti-interleukin-1 beta effects of anti-rheumatic drugs.
从骨关节炎和类风湿性关节炎患者样本中制备的滑膜细胞培养物，用不同的抗炎剂（皮质醇、吲哚美辛、布洛芬和吡罗昔康）进行处理，以确定它们的“抗白细胞介素-1β”作用，采用抑制白细胞介素-1β介导的葡萄糖摄取刺激作为生物学检测方法。汇合的细胞用不同浓度的这些药物（10⁻⁵、10⁻⁶和10⁻⁷mol/L）处理24小时，以研究它们对炎症过程的影响。在进行葡萄糖摄取研究前6小时，加入白细胞介素-1β（1 ng/ml）。非甾体抗炎剂无效，而皮质醇抑制白细胞介素-1β对葡萄糖摄取的作用。在骨关节炎细胞中，10⁻⁵mol/L的皮质醇在孵育24小时后，使白细胞介素-1β介导的葡萄糖摄取降低了27%。在类风湿性细胞中，刺激后的2-脱氧-D-葡萄糖摄取降低了40.6%。当在测量葡萄糖摄取前6小时同时加入白细胞介素-1β和皮质醇时，结果相似。皮质醇的这种快速作用依赖于蛋白质合成（被放线菌酮抑制）。皮质醇通过作用于基础的和白细胞介素-1β介导的葡萄糖摄取，降低滑膜细胞的葡萄糖摄取。这种作用在类风湿性滑膜细胞中更明显。抑制白细胞介素-1β介导的葡萄糖摄取可被提议作为研究抗风湿药物抗白细胞介素-1β作用的一种新模型。
