Ibuprofen: New explanation for an old phenomenon

Nuclear factor-kappa B (NF-kappa B) 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-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). 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-1 beta and TNF-alpha. 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-kappa B by blocking the degradation of inhibitor-kappa B alpha, a protein that forms a complex with transcription factor NF-kappa B by blocking the degradation of inhibitor-kappa B alpha, a protein that forms a complex with NF-kappa B, thereby preventing the release and subsequent translocation of NF-kappa B into the nucleus and the expression of inflammatory cytokines. The presented data offer a new explanation for the anti-inflammatory effect of ibuprofen. (C) 1998 Elsevier Science Inc.