Abstract
Tumor necrosis factor-alpha (TNF-alpha) has a central role in inflammation and is modulated by prostaglandin E(2) (PGE(2)) and cyclic adenosine monophosphate (cAMP). Using microarray, quantitative real-time polymerase chain reaction (qRT-PCR), and protein detection techniques, we showed that ketorolac and rofecoxib had no significant effect on TNF-alpha gene expression in oral mucosal biopsies 3 h after surgery. They both, however, downregulated the gene and protein expression of phosphodiesterase type 4 (PDE4D), which might represent a novel mechanism contributing to their analgesic and anti-inflammatory effects.
Publication types
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Comparative Study
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Randomized Controlled Trial
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Research Support, N.I.H., Intramural
MeSH terms
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Adolescent
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Adult
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Cyclic Nucleotide Phosphodiesterases, Type 3 / biosynthesis*
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Cyclic Nucleotide Phosphodiesterases, Type 3 / genetics
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Cyclic Nucleotide Phosphodiesterases, Type 4
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Cyclooxygenase Inhibitors / pharmacology*
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Cyclooxygenase Inhibitors / therapeutic use
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Down-Regulation / drug effects*
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Down-Regulation / physiology
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Gene Expression Regulation, Enzymologic / drug effects*
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Gene Expression Regulation, Enzymologic / physiology
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Humans
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Inflammation / drug therapy
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Inflammation / enzymology
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Inflammation / genetics
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Pain / drug therapy
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Pain / enzymology*
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Pain / genetics
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Phosphodiesterase 3 Inhibitors*
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Tumor Necrosis Factor-alpha / biosynthesis
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Tumor Necrosis Factor-alpha / genetics
Substances
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Cyclooxygenase Inhibitors
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Phosphodiesterase 3 Inhibitors
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Tumor Necrosis Factor-alpha
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Cyclic Nucleotide Phosphodiesterases, Type 3
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Cyclic Nucleotide Phosphodiesterases, Type 4
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PDE4D protein, human