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Arachidonic acid strongly stimulates prostaglandin I3 (PGI3) production from eicosapentaenoic acid in human endothelial cells
Authors:J C Bordet  M Guichardant  M Lagarde
Institution:1. BioScience Research Centre, Visakapatnam, India;2. UND Life Sciences, Battle Ground, USA;1. Research Center on Aging, Health and Social Services Center, University Institute of Geriatrics of Sherbrooke, Sherbrooke, Canada J1H 4C4;2. Departement of Medicine, Université de Sherbrooke, Sherbrooke, Canada;3. Institute of Nutrition and Functional Foods, Université Laval, Québec, Canada;4. Faculty of pharmacy, Université Laval and CHU-Q Research Centre, Québec, Canada;1. School of Food and Nutrition, Massey University, Auckland, New Zealand;2. School of Food and Nutrition, Massey University, Palmerston North, New Zealand;1. Division of Allergy-Immunology, Northwestern University Feinberg School of Medicine, Chicago, Ill;2. Ann & Robert H. Lurie Children''s Hospital of Chicago, Chicago, Ill;1. Institute of Cardiovascular Research and Sports Medicine, Department of Molecular and Cellular Sports Medicine, German Sport University, Cologne, Germany;2. Department of Safety and Quality of Fruit and Vegetables, Max Rubner-Institut, Karlsruhe, Germany, Germany;3. State Key Laboratory of Food Science and Technology, Nanchang University, China;4. Clinic for Cattle, Endocrinology, University of Veterinary Medicine, Hannover, Germany;1. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA;2. Public Health, Department of Social Medicine, Osaka University Graduate School of Medicine, Osaka, Japan;3. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA;4. Department of Epidemiology, University of Washington, Seattle, WA, USA
Abstract:Eicosapentaenoic acid (EPA) is a prominent polyunsaturated fatty acid in fish oil which inhibits blood platelet aggregation and thromboxane A2 formation but not prostacyclin-like material generation from vascular endothelium. In this study we investigated interaction between EPA and arachidonic acid (AA) during their oxygenation by cultured endothelial cells. As measured by gas chromatography-mass spectrometry (GC-MS), AA increased markedly prostaglandin I3 (PGI3) production from EPA while that of PGI2 from AA was decreased by EPA. However, increasing the ratio AA/EPA over one almost suppressed the inhibition of PGI2 formation by EPA, and the stimulation of PGI3 production by AA was even higher. The effect of AA on EPA conversion to minor prostaglandins like PGE3 and PGF3 alpha was similar then confirming the stimulating effect and suggesting it is occurring at the cyclooxygenase instead of the prostacyclin synthase level. Altogether these data indicate that, in certain nutritional states where the liberation of EPA from endothelial cells will be accompanied with that of endogenous AA, substantial amounts of PGI3 could contribute to the prostacyclin-like activity of the vessel wall in addition to PGI2.
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