http://www.cnr.it/ontology/cnr/individuo/prodotto/ID23859
The omega-3 fatty acid docosahexaenoate attenuates endothelial cyclooxygenase-2 induction through both NADP(H) oxidase and PKC epsilon inhibition (Articolo in rivista)
- Type
- 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
- 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)
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- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni
- http://www.pnas.org/content/103/41/15184.long (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
- 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
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- 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 HospitalHarvard 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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