文摘
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Summary
Omega-3 fatty acids (¦Ø-3 FAs) have potential anti-inflammatory activity in a variety of inflammatory human diseases, but the mechanisms remain poorly?understood. Here we show that stimulation of macrophages with ¦Ø-3 FAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and other family members, abolished NLRP3 inflammasome activation and inhibited subsequent caspase-1 activation and IL-1¦Â secretion. In addition, G protein-coupled receptor 120 (GPR120) and?GPR40 and their downstream scaffold protein ¦Â-arrestin-2 were shown to be involved in inflammasome inhibition induced by ¦Ø-3 FAs. Importantly, ¦Ø-3?FAs also prevented NLRP3 inflammasome-dependent inflammation and metabolic disorder in a high-fat-diet-induced type 2 diabetes model. Our?results reveal a mechanism through which ¦Ø-3 FAs repress inflammation and prevent inflammation-driven diseases and suggest the potential clinical use of ¦Ø-3 FAs in gout, autoinflammatory syndromes, or other NLRP3 inflammasome-driven inflammatory diseases.
