Abstract
Nuclear factor-κB (NF-κB) and activating protein-1 (AP-1) play an important role in the induction of pro-inflammatory factors such as cytokines and cell adhesion molecules, which could be involved in the pathogenesis of inflammatory diseases. In vitro study using cultured cells have suggested that these transcription factors are possible molecular targets for the anti-inflammatory action of steroids. However, the precise molecular mechanisms of the therapeutic effects of steroids on inflammatory diseases in vivo are not yet fully understood. Here, we show the suppressive effects of steroids on NF-κB and AP-1 activation in rat experimental glomerulonephritis induced by nephrotoxic serum (NTS), and discuss the recent approaches for the development of novel anti-inflammatory agents controlling NF-κB and AP-1 activation.
