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

Figure 7 Allyl isothiocyanate ameliorates lipid accumulation by activating the Sirt1/AMPKα signaling pathway. After transfection with Sirtuin 1 (Sirt1) small interfering RNA (siRNA), AMP-activated protein kinase α (AMPKα) siRNA or the corresponding scrambled control for 48 h, AML-12 cells were incubated in normal medium or medium containing palmitate acid (PA) with or without allyl isothiocyanate (AITC) for 24 h. A: Three different Sirt1 siRNA sequences were used, and Sirt1 protein levels were examined by western blot analysis. In the following experiments, we selected Sirt1 siRNA #3. B: Intracellular triglyceride (TG) content in AML-12 cells (n = 4/group). C: Sirt1, phosphorylated AMPKα and proliferator-activated receptor gamma coactivator1α (PGC1α) protein expression was detected by western blot analysis. D: Three different AMPKα siRNA sequences were used, and AMPKα protein levels were examined by western blot analysis. In the subsequent experiments, we selected AMPKα siRNA #3. (E) Intracellular TG content in AML-12 cells (n = 4/group). Data are presented as the mean ± SD. ^aP < 0.05, ^bP < 0.01 vs Control siRNA + PA, ^dP < 0.01 vs Control siRNA + PA + AITC, ^fP < 0.01 vs Control siRNA + PA, ^hP < 0.01 vs Control siRNA + PA + AITC. PA: Palmitate acid; AITC: Allyl isothiocyanate; PGC1α: Proliferator-activated receptor gamma coactivator 1α; Sirt1: Sirtuin 1; AMPKα: AMP-activated protein kinase α; p-AMPKα: Phosphorylated AMP-activated protein kinase α; TG: Triglyceride.