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Last Updated: 3 years ago

Possible Interaction: Eicosapentaenoic Acid and Epoprostenol

Research Papers that Mention the Interaction

The levels of leukotriene B4, thromboxane A2, and prostaglandin I2 were significantly lower in patients receiving EPA than in those not receiving it (all P < 0.01).
Bone Marrow Transplantation  •  2001  |  View Paper
Like the endothelial cultures, intact mouse brain microvessels convert EPA into eicosanoids, and incubation with EPA reduces the subsequent capacity of the microvessels to produce PGI2 and PGE2.
Journal of lipid research  •  1989  |  View Paper
These results indicate that there is an interspecies difference in the sensitivity of IPA to NE and PGI2.
Prostaglandins  •  1985  |  View Paper
In rat, EPA was not only being converted to no PGI3, but also being a blocker to PGI2 synthesis in vascular cells.
Thrombosis research  •  1983  |  View Paper
Compared with DHA, EPA administration increases the EPA/AA ratio and the ( PGI2 + PGI3)/TXA2 balance to a state that inhibits the onset and/or progression of CVD.
Journal of atherosclerosis and thrombosis  •  2013  |  View Paper
Administration of EPA increased PGI2 production in the rat thoracic aorta and co-culture of rat aorta smooth muscle cell with EPA also increased PGI2 production, but suppressed smooth muscle cell proliferation.
Nihon rinsho. Japanese journal of clinical medicine  •  1992  |  View Paper
EPA appears to decrease the capacity of the endothelial cells to produce PGI2 in two ways: by reducing the arachidonic acid content of the cell phospholipid precursor pools and by acting as an inhibitor of prostaglandin production.
Journal of lipid research  •  1983  |  View Paper
Additionally, EPA bound to the α-position of TAG increased the ratio of PGI2 to TXA2 to a higher degree than EPA bound to the β-position.
The Journal of nutritional biochemistry  •  2015  |  View Paper
These results indicate that dietary AA stimulates and dietary EPA reducesin vivo PGI2 production in the rat.
Lipids  •  2006  |  View Paper
EPA more strongly inhibits the formation of this product than the release of PGI2 from ears after incorporation of 14C-AA.
Naunyn-Schmiedeberg's Archives of Pharmacology  •  2004  |  View Paper
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