Fig. 3 A summary of the anti-inflammatory mechanisms of n-3 PUFAs. (A) N-3 PUFAs can regulate expression of inflammatory cytokines, chemokines and adhesion molecules, inhibit NLRP3 inflammasomes, activate anti-inflammatory transcription factors (PPARα/γ) and activate GPR120 receptors which inhibit TLR4-mediated activation of NF-κB. (B) N-3 PUFAs are metabolized by COX/5-LOX into 5-series LTs which exert anti-inflammatory effects. (C) N-3 PUFAs can replace n-6 PUFAs, such as AA, altering the inflammatory response. N-3 PUFA will alter cell membrane composition, fluidity and mediated signaling. (D) N-3 PUFAs, DHA and EPA, are metabolized by CYP epoxygenases into bioactive epoxylipids with anti-inflammatory properties. (E) N-3 PUFAs are metabolized by COX/LOX into SPMs which act as potent anti-inflammatory modulators. AA, Arachidonic acid; CCL, Chemokine ligand; COX, Cyclooxygenase; CYP, Cytochrome P450; DHA, Docosahexaenoic acid; EDP, Epoxydocosapentaenoic acid; EEQ, Epoxyeicosatetraenoic acid; EPA, Eicosapentaenoic acid; GRP, G-protein coupled receptor; IL, Interleukin; LOX, Lipoxygenase; LT, Leukotriene; PUFA, Poly unsaturated fatty acid; NFκB, Nuclear factor kappa-light-chain enhancer activated B-cells; NLRP3, NACHT, LRR and PYD domains-containing protein 3; PLA2, Phospholipase A2; PMN, Polymorphonuclear neutrophils; PPAR, Peroxisome proliferator-activated receptor; ROS, Reactive oxygen species; SPMs, Specialized pro-resolving mediators; TLR, Toll like receptor; TNF-α, Tumor necrosis factor-α.