期刊
IMMUNITY
卷 38, 期 6, 页码 1154-1163出版社
CELL PRESS
DOI: 10.1016/j.immuni.2013.05.015
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资金
- NSFC [81222040, 81273318, 31200659, 91029303]
- National Basic Research Program of China [2013CB944904]
- Chinese Academy of Sciences, the Doctoral Fund of Ministry of Education of China [20123402120001, 20123402110010]
- Program for New Century Excellent Talents in University
- Fundamental Research Funds for the Central Universities
- University of Science and Technology of China
- Swiss National Science Foundation
- NCCR Molecular Oncology
- Foundation Louis-Jeantet
- EU-FP7 program APO-SYS
- Institute for Arthritis Research
- Swiss National Science Foundation [PP00P3_ 139094]
- Swiss National Science Foundation (SNF) [PP00P3_139094] Funding Source: Swiss National Science Foundation (SNF)
Omega-3 fatty acids (omega-3 FAs) have potential antiinflammatory activity in a variety of inflammatory human diseases, but the mechanisms remain poorly understood. Here we show that stimulation of macrophages with omega-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 beta secretion. In addition, G protein-coupled receptor 120 (GPR120) and GPR40 and their downstream scaffold protein beta-arrestin-2 were shown to be involved in inflammasome inhibition induced by omega-3 FAs. Importantly, u-3 FAs also prevented NLRP3 inflammasomedependent inflammation and metabolic disorder in a high-fat-diet-induced type 2 diabetes model. Our results reveal a mechanism through which u-3 FAs repress inflammation and prevent inflammation- driven diseases and suggest the potential clinical use of omega-3 FAs in gout, autoinflammatory syndromes, or other NLRP3 inflammasome-driven inflammatory diseases.
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