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  • Title: Oxidized omega-3 fatty acids inhibit NF-kappaB activation via a PPARalpha-dependent pathway.
    Author: Mishra A, Chaudhary A, Sethi S.
    Journal: Arterioscler Thromb Vasc Biol; 2004 Sep; 24(9):1621-7. PubMed ID: 15231516.
    Abstract:
    OBJECTIVE: The aim of this study was to determine the effects of oxidized versus native omega-3 fatty acids on the endothelial expression of chemokines MCP-1 and IL-8, and, if effective in inhibiting chemokine expression, to determine the mechanism for the inhibition of chemokine expression. METHODS AND RESULTS: Using enzyme-linked immunosorbent assays, we show that oxidized EPA and DHA but not unoxidized EPA or DHA inhibit cytokine-induced endothelial expression of monocyte chemoattractant protein (MCP)-1 and, to a lesser extent, IL-8. In electrophoretic mobility shift assays, oxidized EPA but not unoxidized EPA potently inhibited cytokine-induced activation of endothelial nuclear factor-kappaB (NF-kappaB). Using Western blot analyses, we show that the inhibition of NF-kappaB activation was not caused by prevention of phosphorylation of IkappaBalpha because oxidized EPA did not inhibit cytokine-induced phosphorylation and ubiquination of IkappaBalpha. Furthermore, oxidized EPA inhibited NF-kappaB activation in endothelial cells derived from wild-type mice but had no inhibitory effects on NF-kappaB activation in endothelial cells derived from peroxisome proliferator-activated receptor alpha (PPARalpha)-deficient mice, indicating that oxidized EPA requires PPARalpha for its inhibitory effects on NF-kappaB. CONCLUSIONS: These studies show that the antiinflammatory effects of fish oil may result from the inhibitory effects of oxidized omega-3 fatty acids on NF-kappaB activation via a PPARalpha-dependent pathway.
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