N-Acetylcysteine enhances the action of anti-inflammatory drugs as suppressors of prostaglandin production in monocytes

THE anti-inflammatory effect of non-steroidal anti-inflammatory drugs (NSAIDs) is associated with inhibition of cyclooxygenase (COX), the rate-limiting enzyme responsible for the synthesis of prostaglandins. Since oxygen free radicals can act as second cellular messengers, especially to modulate the...

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Bibliographic Details
Published in:Mediators of Inflammation 2002-10, Vol.2002 (5), p.321-323
Main Authors: Hoffer, Erica, Baum, Yelena, Nahir, A Menahem
Format: Article
Language:English
Subjects:
Acetylcysteine - pharmacology
Anti-Inflammatory Agents, Non-Steroidal - pharmacology
Diclofenac - pharmacology
Dinoprostone - biosynthesis
Drug Synergism
Expectorants - pharmacology
Humans
In Vitro Techniques
Lactones - pharmacology
Lipopolysaccharides - pharmacology
Monocytes - drug effects
Monocytes - metabolism
Sulfones
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Summary:THE anti-inflammatory effect of non-steroidal anti-inflammatory drugs (NSAIDs) is associated with inhibition of cyclooxygenase (COX), the rate-limiting enzyme responsible for the synthesis of prostaglandins. Since oxygen free radicals can act as second cellular messengers, especially to modulate the metabolism of arachidonic acid and the prostaglandin tract, it seems plausible that antioxidants might affect the production of prostaglandin by activated cells. This research is focused on the effect of the antioxidant N-acetylcysteine (NAC) on the inhibition of prostaglandin E_2 formation in activated monocytes by specific and non-specific COX inhibitors. We found that lipopolysaccharide-induced prostaglandin E_2 formation was significantly reduced by rofecoxib and by diclofenac, two NSAIDs. Addition of NAC to each of these drugs enhanced the effect of the NSAIDs. These results suggest that one might expect either a potentiation of the anti-inflammatory effect of COX inhibitors by their simultaneous administration with NAC, or obtaining the same anti-inflammatory at lower drug levels.
ISSN:0962-9351
1466-1861
DOI:10.1080/09629350210000015737