%0 Journal Article
%@ 1079-5006
%A Anderson, Rozalyn
%A Cordero, Mario D.
%A Bullón, Pedro
%A Ruiz-Cabello, Jesús
%A Robertson, Avril A B
%A Ryffel, Bernhard
%A Pérez-Pulido, Antonio J
%A Muntané, Jordi
%A Pérez-Alegre, Mónica
%A Andújar-Pulido, Eloísa
%A de la Cruz, Patricia
%A Cooper, Matthew A
%A Lendines-Cordero, Debora
%A Alcocer-Gómez, Elísabet
%A Castejón-Vega, Beatriz
%A Marín-Aguilar, Fabiola
%D 2019
%F uneatlantico:122
%J The Journals of Gerontology: Series A
%K NLRP3 inflammasome; Aging; Autophagy; MCC950; PPARα.
%N 8
%P 1457-1464
%T NLRP3 Inflammasome Inhibition by MCC950 in Aged Mice Improves Health via Enhanced Autophagy and PPARα Activity
%U http://repositorio.uneatlantico.es/id/eprint/122/
%V 75
%X 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.