Regulates macrophage polarization via the lipophage-NLRP3 inflammasome to ameliorate atherosclerosis in ApoE-/- mice.

[Display omitted] • Carnosine could ameliorate atherosclerosis in ApoE^-/- mice. • Carnosine could activate autophagy to inhibit the inflammasome. • Carnosine could activate inhibit the inflammasome to regulate macrophage differentiation. To explore the mechanism of carnosine in improving atherosclerosis, ApoE^-/- mice fed a high-fat diet (HFD) were orally administered different doses of carnosine for 16 weeks. Carnosine intervention significantly reduced the arterial plaque area and expression levels of IL-6, TNF-α, and IL-1β mRNA and increased the expression levels of IL-10 mRNA. Carnosine intervention increased LC3B, Beclin-1, and Atg7 mRNA expression levels and reduced ASC, NLRP3, and Caspase-1 mRNA expression levels. Meanwhile, carnosine could increase Arg-1, CD163, and CD206 mRNA expression levels and decrease iNOS mRNA expression levels. These results suggested that carnosine might regulate macrophage polarization by inhibiting the NLRP3 inflammasome through autophagy to alleviate atherosclerosis, which revealed a novel idea for carnosine to suppress atherosclerosis and offered a scientific foundation for the production of carnosine-enriched dietary products. [ABSTRACT FROM AUTHOR]