Cyclooxygenase inhibition in human monocytes increases endotoxin-induced TNFα without affecting cyclooxygenase-2 expression

Human endotoxin-stimulated adherent monocytes were used in order to determine whether or not NSAIDs influence cyclooxygenase-2 and/or tumor necrosis factor (TNF)α expression within the range of inhibitor concentrations that are required to suppress prostaglandin biosynthesis. Exogenous prostaglandin...

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Bibliographic Details
Published in:European journal of pharmacology 2004-10, Vol.501 (1), p.9-17
Main Authors: Ulcar, Ruth, Peskar, Bernhard A., Schuligoi, Rufina, Heinemann, Akos, Kessler, Harald H., Santner, Brigitte I., Amann, Rainer
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cells, Cultured
Cyclooxygenase
Cyclooxygenase 2
Cyclooxygenase 2 Inhibitors
Cyclooxygenase Inhibitors - pharmacology
Dose-Response Relationship, Drug
Endotoxins - pharmacology
Gene Expression Regulation, Enzymologic - drug effects
Gene Expression Regulation, Enzymologic - physiology
Glucocorticoid
human
Humans
Medical sciences
Membrane Proteins
Monocyte
Monocytes - drug effects
Monocytes - enzymology
NSAID
Pharmacology. Drug treatments
Prostaglandin E 2
Prostaglandin-Endoperoxide Synthases - biosynthesis
Prostaglandin-Endoperoxide Synthases - genetics
Prostaglandin-Endoperoxide Synthases - metabolism
Prostaglandin-Endoperoxide Synthases - physiology
TNFα
Tumor Necrosis Factor-alpha - biosynthesis
Tumor Necrosis Factor-alpha - genetics
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Description
Summary:Human endotoxin-stimulated adherent monocytes were used in order to determine whether or not NSAIDs influence cyclooxygenase-2 and/or tumor necrosis factor (TNF)α expression within the range of inhibitor concentrations that are required to suppress prostaglandin biosynthesis. Exogenous prostaglandin E 2 (IC 50
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2004.08.003