Ibuprofen: new explanation for an old phenomenon

Abstract Nuclear factor-κB (NF-κB) translocation from the cytoplasm into the nucleus and the subsequent DNA binding is an essential prerequisite in the up-regulation of many pro-inflammatory genes, e.g. tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). The anti-inflammatory drug ibuprofen, thought to exert its beneficial effects mainly by suppressing the production of eicosanoids, inhibited the up-regulation of the pro-inflammatory cytokines IL-1β and TNF-α. This effect was independent of the described potential of ibuprofen as a cyclooxygenase inhibitor. Ibuprofen inhibited the activation and translocation of the key transcription factor NF-κB by blocking the degradation of inhibitor-κBα, a protein that forms a complex with NF-κB, thereby preventing the release and subsequent translocation of NF-κB into the nucleus and the expression of inflammatory cytokines. The presented data offer a new explanation for the anti-inflammatory effect of ibuprofen.