Control of cyclooxygenase-2 transcriptional activation by pro-inflammatory mediators.
Cyclooxygenase-2 (COX-2) plays a key role in diverse inflammatory conditions. Its cellular levels depend on transcriptional activation by pro-inflammatory mediators. The mechanism by which phorbol esters and cytokines activate COX-2 gene expression has been extensively characterized. Several endogenous molecules and natural products have been reported to inhibit COX-2 expression by targeting at the transcriptional activation induced by pro-inflammatory mediators. This review highlights the importance of C/EBP beta and NF-kappa B in COX-2 transcriptional activation by proinflammatory mediators and as targets of inhibition by endogenous molecules such as melatonin and natural products including salicylate and polyphenols.
Wu
K K
KK
Vascular Biology Research Center and Division of Hematology, Department of Internal Medicine, Institute of Molecular Medicine and Medical School, University of Texas Health Science Center at Houston, TX 77030, USA. kenneth.k.wu@uth.tmc.edu
D000818:Animals; D022762:CCAAT-Enhancer-Binding Proteins / Q000502:physiology; D051546:Cyclooxygenase 2; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology*; D008550:Melatonin / Q000494:pharmacology; D008565:Membrane Proteins; D016328:NF-kappa B / Q000502:physiology; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics*; D015533:Transcriptional Activation / Q000187:drug effects*
D022762:CCAAT-Enhancer-Binding Proteins; D018836:Inflammation Mediators; D008565:Membrane Proteins; D016328:NF-kappa B; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D008550:Melatonin