Figure 2.

Dotted line, inhibit; solid line, activate. EPA, eicosapentaenoic acid; DHA, docosahexaenoic acid; GPR120, G protein-coupled receptor 120; JNK, JUN NH₂-terminal kinase; TLR-4, toll-like-receptor 4; NF-κB, nuclear factor kappa-β; PPARγ, peroxisome proliferator-activated receptor γ; AA, arachidonic acid; PGE₂, prostaglandins E2. Anti-inflammatory mechanisms of EPA and DHA. EPA and DHA inhibit NF-κB and JNK through binding with GPR120. Incorporation of these n-3 PUFA disrupts the translocation of TLR-4 into lipid raft, thus inactivates NF-κB pathway. Besides, EPA and DHA interfere with the TLR-4 signaling pathway via the downregulation of NADPH oxidase production, which results in the inhibition of NF-κB pathway. These fatty acids also activate PPARγ and, result in the upregulation of adiponectin and leptin secretion. In addition, the intake of EPA and DHA leads to antagonism of n-6 fatty acid arachidonic acid (AA).