Fig. 4

ACLY under NF-kB ACLY-induced transcriptional control in TNFα triggered hepatocytes. A HepG2 cells were transiently transfected for 48 h with pGL3 basic-LUC vectors containing the − 3116/ − 20 bp full-length region of the ACLY gene promoter (3000) or a truncated version of this region (1000). Then, cells were triggered by 5 ng/mL TNFα in the absence (TNFα) or in the presence of 500 μM HCA (TNFα + HCA). Unstimulated cells were used as a negative control (3000 or 1000). The luciferase gene reporter activity was assessed after 24 h. Data were analyzed by one-way ANOVA followed by Tukey’s multiple comparison test. Different letters indicate significant differences between treatments at p < 0.05. B TNFα triggered HH in the presence or absence of HCA were used to carry out chromatin immunoprecipitation (ChIP) analysis with an antibody against subunit p65 of NF-κB. Data are representative of 3 independent experiments and are presented as means ± SD (error bars). Different letters above the bars indicate significant differences between treatments at p < 0.05, according to Tukey’s post hoc test performed after one-way ANOVA