Problems and results in testing the possible general mode of action of glucocorticoids in rat adjuvant arthritis.

The antiinflammatory action of dexamethasone in both phases of rat adjuvant arthritis was significantly reduced by injection of the RNA synthesis inhibitor actinomycin D into the inflamed paw. This effect is apparently caused by inhibition of RNA/protein synthesis and not by actinomycin D irritant activity. Thus, the present data support the view of indirect glucocorticoid activity via gene expression also in subacute and chronic adjuvant arthritis. The dexamethasone-induced antiinflammatory protein seems to be synthetized at the site of inflammation.