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pubmed-article:18067925pubmed:abstractTextOmega-3 fatty acids (n-3 FA) demonstrate significant anti-inflammatory properties thought to occur through three principal mechanisms; (1) displacement of arachidonic acid from the cellular membrane, (2) differential prostaglandin E2 (PGE2) and LTB4 production, and (3) molecular level alterations such as diminished nuclear factor kappa B and AP-1 activation. Recently, n-3 FA have been demonstrated to significantly decrease nitric oxide (NO) production in a lipopolysaccharide (LPS)-stimulated M Phi model. We hypothesized that decreased NO production by n-3 FA occurs through inhibition of cyclooxygenase-2 (COX-2) derived PGE2 and that repletion of the system with PGE2 would obliterate these effects. Selective COX-2 inhibitor (L-748,731) experiments and separate PGE2 repletion studies were used to test this hypothesis.lld:pubmed
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pubmed-article:18067925pubmed:articleTitleAttenuation of iNOS in an LPS-stimulated macrophage model by omega-3 fatty acids is independent of COX-2 derived PGE2.lld:pubmed
pubmed-article:18067925pubmed:affiliationDepartment of Surgery, University of Illinois at Chicago, Chicago, Illinois 60612, USA.lld:pubmed
pubmed-article:18067925pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18067925pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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