Abstract
Cyclooxygenase-2 may play a role in resolution of carrageenan-induced pleurisy in rats by generating anti-inflammatory prostanoids. Here, we show exudate prostaglandin F2alpha concentrations rise during resolution of this model. These were reduced by the selective cyclooxygenase-2 inhibitor NS-398, which exacerbated inflammation. Concomitant treatment with NS-398 and the synthetic FP receptor agonist fluprostenol reversed this exacerbation. This suggests prostaglandin F2alpha produced by cyclooxygenase-2 contributes to resolution of this inflammatory reaction.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Cyclooxygenase 2 / metabolism*
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Cyclooxygenase Inhibitors / pharmacology
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Cyclooxygenase Inhibitors / toxicity
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Dinoprost / biosynthesis*
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Inflammation / chemically induced
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Inflammation / drug therapy
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Inflammation / metabolism*
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Nitrobenzenes / pharmacology
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Nitrobenzenes / toxicity
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Pleurisy / chemically induced
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Pleurisy / drug therapy
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Pleurisy / metabolism
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Prostaglandins F, Synthetic / pharmacology
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Rats
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Rats, Wistar
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Receptors, Prostaglandin / antagonists & inhibitors
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Sulfonamides / pharmacology
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Sulfonamides / toxicity
Substances
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Cyclooxygenase Inhibitors
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Nitrobenzenes
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Prostaglandins F, Synthetic
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Receptors, Prostaglandin
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Sulfonamides
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prostaglandin F2alpha receptor
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N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide
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fluprostenol
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Dinoprost
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Cyclooxygenase 2