Regular ArticleRole of Ca2+-Independent Phospholipase A2 and Cyclooxygenase/Lipoxygenase Pathways in the Nitric Oxide Production by Murine Macrophages Stimulated by Lipopolysaccharides
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2015, Fish and Shellfish ImmunologyCitation Excerpt :In the current trial, the combination AA + EPA upregulated CD36 expression while supplementation with the other fatty acid combinations had no effect. PPARs are activated by fatty acids, as PPARs are ligands for mediators in the eicosanoid pathway in leukocytes of mice [51,52] and humans [53]. In this study, PPAR was also upregulated when adding AA + EPA to the cells while acyl coenzyme A oxygenase (ACO) was down-regulated.
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2014, Chemico-Biological InteractionsCitation Excerpt :Thus, combined with their data, we concluded that AA inhibits iNOS-dependent NO production by suppressing binding of NF-κB to the promoter region of the iNOS gene in MES-13 cells. Vivancos and Moreno have reported PGE2 via EP4 receptor/cAMP signaling was involved in NO release induced by LPS in macrophages RAW 264.7 cultures [36]. Since AA modulates PLA2 activity and eicosanoid release [37,38] and EP4 has been identified as the major PGE2 receptor in MES-13 cells [39], we also investigated the effect of AA on PGE2 production in MES-13 cells.
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