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J Gerontol A Biol Sci Med Sci ; 75(8): 1457-1464, 2020 07 13.
Article in English | MEDLINE | ID: mdl-31603987

ABSTRACT

The NLRP3 inflammasome has emerged as an important regulator of metabolic disorders and age-related diseases in NLRP3-deficient mice. In this article, we determine whether, in old mice C57BL6J, the NLRP3 inflammasome inhibitor MCC950 is able to attenuate age-related metabolic syndrome to providing health benefits. We report that MCC950 attenuates metabolic and hepatic dysfunction in aged mice. In addition, MCC950 inhibited the Pi3K/AKT/mTOR pathway, enhanced autophagy, and activated peroxisome proliferator-activated receptor-α in vivo and in vitro. The data suggest that MCC950 mediates the protective effects by the mammalian target of rapamycin inhibition, thus activating autophagy and peroxisome proliferator-activated receptor-α. In conclusion, pharmacological inhibition of NLRP3 in aged mice has a significant impact on health. Thus, NLRP3 may be a therapeutic target of human age-related metabolic syndrome.


Subject(s)
Autophagy/drug effects , Heterocyclic Compounds, 4 or More Rings/pharmacology , Inflammasomes/antagonists & inhibitors , NLR Family, Pyrin Domain-Containing 3 Protein/antagonists & inhibitors , PPAR alpha/drug effects , Sulfones/pharmacology , Aging , Animals , Fatty Liver/prevention & control , Furans , Gene Expression , Indenes , Lipids/blood , Liver/metabolism , Mice, Inbred C57BL , Proto-Oncogene Proteins c-akt/drug effects , Sulfonamides , TOR Serine-Threonine Kinases/drug effects
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