Diallyl trisulfide inhibits 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung cancer via modulating gut microbiota and the PPARγ/NF-κB pathway

Abstract

DATS ameliorated NNK-induced lung tumorigenesis by the modulation of gut microbiota and regulation of the PPARγ/NF-κB signaling pathway, thereby reducing the accumulation of inflammatory factors.