Allyl isothiocyanate ameliorates lipid accumulation and inflammation in nonalcoholic fatty liver disease via the Sirt1/AMPK and NF-κB signaling pathways

Figure 2 Allyl isothiocyanate upregulates the expression of proteins involved in fatty acid β-oxidation, downregulates the protein levels of lipogenesis genes, and activates the Sirtuin 1/AMP-activated protein kinase signaling pathway in the liver tissues of high fat diet-fed mice. A: The protein expression of sterol regulatory element­binding protein 1 (SREBP1), its lipogenesis target genes (SCD1 and FAS), and genes involved in fatty acid β-oxidation, such as proliferator-activated receptor gamma coactivator 1α (PGC1α), peroxisome proliferator-activated receptor α (PPARα) and carnitine palmitoyltransferase 1 α (CPT1α), was detected by western blot analysis. B: Sirtuin 1 (Sirt1), total and phosphorylated AMP-activated protein kinase α (AMPKα) protein expression was detected by western blot analysis. ^aP < 0.05, ^bP < 0.01 vs HFD(+) AITC(-). PGC1α: Proliferator-activated receptor gamma coactivator 1α; PPARα: Peroxisome proliferator-activated receptor α; CPT1α: Carnitine palmitoyltransferase 1 α; SREBP1: Sterol regulatory element­binding protein 1; SCD1: Stearoyl coenzyme A desaturase 1; FAS: Fatty acid synthase; Sirt1: Sirtuin 1; AMPKα: AMP-activated protein kinase α; p-AMPKα: Phosphorylated AMP-activated protein kinase α; HFD: High fat diet; AITC: Allyl isothiocyanate.