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. 2021 Apr 27;296:100714. doi: 10.1016/j.jbc.2021.100714

Figure 2.

Figure 2

Pharmacological inhibition of NF-κB p65 attenuates high glucose-induced hepatic lipid accumulation.A and B, qualitative and quantitative representation of NF-κB p65 in the subcellular fractionation lysates of cells treated with depicted conditions (B, mean ± SEM, ∗∗p < 0.005). C and D, immunofluorescence images of subcellular localization of ChREBP in presence PDTC or NF-κB p65 siRNA under low/high glucose conditions via immunocytochemistry in HepG2 cells (Image scale bar is 10 μm), with the quantification of ChREBP signals (nuclear: cytoplasmic ratio). E and F, representative microscopic images of Bodipy staining of HepG2 cells depicting abundance of intracellular lipid droplets in different conditions as depicted, inferring the extent of lipogenesis (Image scale bar is 10 μm) (F, mean ± SEM, ∗p < 0.05, ∗∗∗p < 0.0005). ChREBP, carbohydrate response element-binding protein; NF-κB, nuclear factor kappa-light chain enhancer of activated B cells; PDTC, pyrrolidine dithiocarbamate.