Research Paper Volume 16, Issue 5 pp 4095—4115

FoxO6-mediated ApoC3 upregulation promotes hepatic steatosis and hyperlipidemia in aged rats fed a high-fat diet

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Figure 5. Deficiency of ApoC3 suppressed FoxO6-mediated lipid accumulation in AC2F liver cells. (A) AC2F cells were transiently transfected with ApoC3-siRNA (20 nM) for 24 h with or without FoxO6 (100 MOI). Cells were analyzed using western blotting using antibodies against FoxO6, ApoC3, and β-actin. Bars in the densitometry data represent the mean ± S.E., and significance was determined using one-factor ANOVA: #p < 0.05, ##p < 0.01, ###p < 0.001 vs. Normal; **p < 0.01 vs. FoxO6-CA. (B) Levels of ApoC3 were determined in the media of the cells. Three independent experiments were performed and similar results were obtained. Results of one-factor ANOVA: **p < 0.01 vs. non-treated cells; ##p < 0.01 vs. FoxO6 virus-treated cells. (C) TG level of the media from FoxO6 with ApoC3-siRNA-treated cells. (D) Cellular TG concentration, after transfected cells were pre-incubated with ApoC3-siRNA (20 nM) for 24 h with or without FoxO6 (100 MOI), was measured using a colorimetric assay. Results of one-factor ANOVA: #p < 0.05, ###p < 0.001 vs. non-treated cells; *p < 0.05, ***p < 0.001 vs. FoxO6 virus-treated cells.