| Literature DB >> 9890559 |
K M Stuhlmeier1, H Li, J J Kao.
Abstract
Nuclear factor-kappaB (NF-kappaB) 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-1beta (IL-1beta). 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-1beta 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-kappaB by blocking the degradation of inhibitor-kappaBalpha, a protein that forms a complex with NF-kappaB, thereby preventing the release and subsequent translocation of NF-kappaB into the nucleus and the expression of inflammatory cytokines. The presented data offer a new explanation for the anti-inflammatory effect of ibuprofen.Entities:
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Year: 1999 PMID： 9890559 DOI： 10.1016/s0006-2952(98)00301-3
Source DB: PubMed Journal: Biochem Pharmacol ISSN： 0006-2952 Impact factor: 5.858