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

Figure 6 Allyl isothiocyanate downregulates the mRNA levels of proinflammatory markers and inhibits the IκB kinase /nuclear factor kappa B signaling pathway in vitro. A: Palmitate acid (PA) (200 μmol/L)-stimulated AML-12 cells were treated with allyl isothiocyanate (AITC) (20 μmol/L) or dimethyl sulfoxide (DMSO) (vehicle) for 6 h (n = 3/group). The mRNA levels of proinflammatory cytokines were measured by quantitative real-time PCR. (B) PA (200 μmol/L)-stimulated AML-12 cells were treated with AITC (20 μmol/L) or DMSO (vehicle) for 24 h. The protein expression of phosphorylated p65, p65, phosphorylated IκB kinase (IKK), IKKα, IKKβ, total and phosphorylated inhibitor of nuclear factor kappa B α (IκB α) was detected by western blot analysis. Data are presented as the mean ± S.D. ^aP < 0.05, ^bP < 0.01 vs PA(+) AITC(-). TNFα: Tumor necrosis factor α; IL-6: Interleukin-6; PA: Palmitate acid; AITC: Allyl isothiocyanate; p-p65: Phosphorylated p65; IKK: IκB kinase; IκBα: Inhibitor of nuclear factor kappa B α.