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Last Updated: 4 years ago

Possible Interaction: Arachidonic Acid and Cyclooxygenase 2 Inhibitors

Research Papers that Mention the Interaction

For instance, nonsteroidal anti‐inflammatory agents (NSAIDs), both classical nonselective (cNSAIDs) and the selective COX‐2 inhibitors coxibs ) attenuate the generation of PGH2 from AA that in turn reduces the synthesis of PGE2 and modifies the inflammatory conditions.
Medicinal research reviews  •  2014  |  View Paper
However, gastrointestinal (GI) and cardiovascular adverse effects of NSAIDs and coxibs , and recent findings demonstrating that there are significant risks from the disruption of oxylipin levels when pharmacologically inhibiting a single ARA cascade metabolic pathway, have led to studies involving the simultaneous inhibition of multiple pathways in ARA cascade.
Current medicinal chemistry  •  2013  |  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
Likewise, the synergism of AA and ADP was, also, attenuated by COX inhibitors (ibuprofen; IC50=20±4 μmol/L and celecoxib; IC50=24±7 μmol/L), PLC inhibitor (U73122; IC50=3.7±0.3 μmol/L), and MAPK inhibitor (PD98059; IC50=2.8±1.1 μmol/L).
Drug design, development and therapy  •  2015  |  View Paper
Interestingly, platelet TXB2 release during aggregation was enhanced after coxib treatment following arachidonic acid or collagen stimulation.
Journal of thrombosis and haemostasis : JTH  •  2007  |  View Paper
Treating the myoblasts with AA and either the COX-1 and COX-2 common inhibitor indomethacin or the COX-2-specific inhibitor NS-398 reversed the stimulatory effect of AA on myoblast proliferation (n = 4, P < 0.05).
Domestic animal endocrinology  •  2019  |  View Paper
Arachidonic acid enhanced both forms of PGE2 release, and a phospholipase A2 inhibitor (amylcinnamoyl anthranilic acid) and COX inhibitors (acetylsalicylic acid and indomethacin) decreased them.
Experimental physiology  •  2006  |  View Paper
In segments of colon mounted in Ussing chambers, arachidonic acid caused a concentration-dependent increase in short-circuit current that was blocked by piroxicam, the COX-2 inhibitor NS-398, and the COX-1 inhibitor SC-560.
The Journal of pharmacology and experimental therapeutics  •  2000  |  View Paper