Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation
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    Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation

  • [2013-07-02]
  •   Recently, the Prof. Rongbin Zhou/Wei Jiang group and Prof. Zhigang Tian group from University of Science&Technology of China, together with the Prof. Jurg Tschopp group from University of Lausanne, reveal a new mechanisms through which Omega-3 fatty acids inhibit inflammation and prevent type 2 diabetes (T2D). The paper entitled with “Omega-3 Fatty Acids Prevent Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome Activation” has been published on《Immunity》in June, 2013. This work has also been highlighted in the same issue of the journal.
       The inflammasome is a cytosolic protein complex composed of nucleotide-binding domain and leucine-rich repeat containing proteins (NLRs), ASC and caspase-1, and plays an important role in the maturation and release of several proinflammatory cytokines, including interleukin-1β (IL-1β), IL-18, and IL-33. The inflammasome is involved in the pathogenesis of several inflammatory disorders, including diabetes, atherosclerosis, and arthritis. Omega-3 fatty acids are not only very important for mental development, but also show potential effects for treatment and prevention of various inflammation-driven diseases. However, the mechanisms remain unclear. In this study, they showed that Omega-3 fatty acids could inhibit NLRP3 inflammasome activation and IL-1b release. As their previous study has shown that NLRP3 inflammasome plays an important role in high-fat diet induced T2D (Nat Immunol, 2010), in this study, they further showed that Omega-3 fatty acids could prevent high-fat diet induced T2D via inhibiting NLRP3 inflammasome activation. These results suggest that NLRP3 inflammasome and its relative signal pathways might be potential targets for treatment of T2D, therefore provide a new clue for designing new drugs for T2D.
       This work was financially supported by National Natural Science Foundation of China, Chinese Academic of Sciences and Ministry of Science and Technology of China.

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