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Last Updated: 3 years ago

Possible Interaction: Arachidonic Acid and Diclofenac

Research Papers that Mention the Interaction

As a non-steroidal anti-inflammatory drug (NSAID), DS binds to both forms of COX (COX-1 and COX-2) and inhibits the conversion of arachidonic acid into pro-inflammatory prostaglandins by means of chelation.
Journal of Chemical Neuroanatomy  •  2018  |  View Paper
In vitro, arachidonic acid and diclofenac synergistically induced neuroblastoma cell death.
Cancer Research  •  2004  |  View Paper
In anesthetized rats treated with bacterial lipopolysaccharide (LPS) to induce the expression … marked increase in PGE2 production that followed bolus intravenous injection of arachidonic acid (3 mg kg−… inhibited by diclofenac but largely unaffected by the COX-2-selective inhibitor …- dimethyl-3-(2-propoxy)-4-methanesulfonylphenyl)-2(5H)-furanone).
Journal of Pharmacology and Experimental Therapeutics  •  2002  |  View Paper
Second, we show that supplying arachidonic acid to increase prostanoid production reduces the effectiveness of both currently used nonsteroidal antiinflammatory drugs (NSAIDs) ( diclofenac ) and novel COX‐2‐selective inhibitors (NS‐398, celecoxib) as inhibitors of COX‐2 activity.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology  •  1999  |  View Paper
Diclofenac , the first nonsteroidal anti-inflammatory agent (NSAID) to be approved that is a phenylacetic acid derivative, competes with arachidonic acid for binding to cyclo-oxygenase, resulting in decreased formation of prostaglandins.
Clinical pharmacy  •  1989  |  View Paper
Instead, by enhancing its reincorporation into triglycerides, diclofenac sodium reduces the intracellular level of free arachidonic acid.
The American journal of medicine  •  1986  |  View Paper
Diclofenac sodium acts by potent cyclo-oxygenase inhibition, reduction of arachidonic acid release , and enhancement of arachidonic acid uptake.
The American journal of medicine  •  1986  |  View Paper
Discussion: Research suggests diclofenac can inhibit the thromboxane-prostanoid receptor, affect arachidonic acid release and uptake, inhibit lipoxygenase enzymes, and activate the nitric oxide–cGMP antinociceptive pathway.
Current medical research and opinion  •  2010  |  View Paper
Diclofenac , along with several others NSAIDs and cyclooxygenase inhibitors, depressed aggregation produced by arachidonic acid in platelet rich plasma from healthy volunteers.
Research communications in molecular pathology and pharmacology  •  2002  |  View Paper
Diclofenac , a phenylacetic acid derivative, is a potent inhibitor of cyclooxygenase enzyme activity, and may also interact with the lipoxygenase enzyme pathway, and with the release and reuptake of arachidonic acid.
Drug intelligence & clinical pharmacy  •  1988  |  View Paper
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