The omega-3 fatty acid docosahexaenoate attenuates endothelial cyclooxygenase-2 induction through both NADP(H) oxidase and PKC epsilon inhibition (Articolo in rivista)

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Label
  • The omega-3 fatty acid docosahexaenoate attenuates endothelial cyclooxygenase-2 induction through both NADP(H) oxidase and PKC epsilon inhibition (Articolo in rivista) (literal)
Anno
  • 2006-01-01T00:00:00+01:00 (literal)
Alternative label
  • Massaro M.; Lubrano L.; Del Turco S.; Lazzerini G.; Bourcier T.; Weksler B. B.; De Caterina R. (2006)
    The omega-3 fatty acid docosahexaenoate attenuates endothelial cyclooxygenase-2 induction through both NADP(H) oxidase and PKC epsilon inhibition
    in Proceedings of the National Academy of Sciences of the United States of America
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Massaro M.; Lubrano L.; Del Turco S.; Lazzerini G.; Bourcier T.; Weksler B. B.; De Caterina R. (literal)
Pagina inizio
  • 15184 (literal)
Pagina fine
  • 15189 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni
  • http://www.pnas.org/content/103/41/15184.long (literal)
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  • 103 (literal)
Rivista
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  • In: Proceedings of the National Academy of Sciences of the United States of America, vol. 103 pp. 15184-15189. National Academy of Sciences, 2006. (literal)
Note
  • Pubme (literal)
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  • Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche, 73100 Lecce, Italy; Departments of Biochemistry and Internal Medicine, American University of Beirut, Beirut, Lebanon; Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche, 56124 Pisa, Italy; Department of Anesthesia, Brigham and Women's Hospital–Harvard Medical School, Boston, MA 02115; Weill Medical College of Cornell University, New York, NY 10021; and Institute of Cardiology and Center of Excellence on Aging, “Gabriele d'Annunzio” University, 66100 Chieti, Italy (literal)
Titolo
  • The omega-3 fatty acid docosahexaenoate attenuates endothelial cyclooxygenase-2 induction through both NADP(H) oxidase and PKC epsilon inhibition (literal)
Abstract
  • A high intake of the omega-3 fatty acid docosahexaenoate [doco- sahexaenoic acid (DHA)] has been associated with systemic anti- inflammatory effects and cardiovascular protection. Cyclooxygen- ase (COX)-2 is responsible for the overproduction of prostaglandins (PG) at inflammatory sites, and its expression is increased in atheroma. We studied the effects of DHA on COX-2 expression and activity in human saphenous vein endothelial cells challenged with proinflammatory stimuli. A >24-h exposure to DHA reduced COX-2 expression and activity induced by IL-1, without affecting COX-1 expression. DHA effect depended on the NF- ? B-binding site in the COX-2 promoter. EMSAs confirmed that DHA attenuated NF- ? B activation. Because MAPK, PKC, and NAD(P)H oxidase all partici- pate in IL-1-mediated COX-2 expression, we also tested whether these enzymes were involved in DHA effects. Western blots showed that DHA blocked nuclear p65 NF- ? B subunit translocation by decreasing cytokine-stimulated reactive oxygen species and ERK1?2 activation by effects on both NAD(P)H oxidase and PKC ? activities. Finally, to address the question whether DHA itself or DHA-derived products were responsible for these effects, we inhibited the most important enzymes involved in polyunsaturated fatty acid metabolism, showing that 15-lipoxygenase-1 products mediate part of DHA effects. These studies provide a mechanistic basis for antiinflammatory and possibly plaque-stabilizing effects of DHA (literal)
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