Action of anti-inflammatory drugs on interleukin-1β-mediated glucose uptake by synoviocytes

Abstract

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-1β’ action, using inhibition of interleukin-1β-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-1β (1 ng/ml) was added. Whereas non-steroid anti-inflammatory agents were inefficient, cortisol inhibited the action of interleukin-1β on glucose uptake. In osteoarthritic cells, cortisol, 10 −5 mol/l, reduced interleukin-1β-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-1β 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-1β-mediated glucose uptake. This effect was more pronounced in rheumatoid synovial cells. The inhibition of interleukin-1β-mediated glucose uptake could be proposed as a new model for studying the anti-interleukin-1β effects of anti-rheumatic drugs.