[Nongenomic effects of glucocorticoids]

The review describes current advances in the knowledge on the mechanisms of glucocorticoid (GC) action. According to the classic genomic model, GCs bind to intracellular receptors and subsequently regulate (directly or indirectly) gene transcription and synthesis of proteins responsible for inflammatory processes. The nongenomic effects of GCs, occur rapidly within seconds or minutes of drug administration, are mediated via a cytosolic but first of all by membrane GC receptors and lead to activation of multiple signal transduction pathways of protein kinases (MAPK, Src, PI3K), cation channels or G protein- -coupled receptors. Nongenomic effects may also occur without receptor involvement. The elucidation of nongenomic actions provides new insights for the understanding of their anti-inflammatory and immunosuppressive GC effects.