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. 2019 Feb 13;41:62–72. doi: 10.1016/j.ebiom.2019.02.019

Fig. 5.

Fig. 5

OA-NO2 inhibits hepatocyte triglyceride accumulation. (a) qPCR analyses of hepatic expression of genes regulating lipid biosynthesis. Data presented in bars are means ± SEM (n = 7–10). (b) Total liver lysates from each experimental group were subjected to western blot analysis of precursor, cleaved SREBP1 and GAPDH as loading control. Quantitative densitometry analysis is shown as box and whiskers from minimum to maximum values showing all points (n = 6). ⁎p < .05, ⁎⁎p < .01, ⁎⁎⁎p < .001 vs CD PEG; ###p < .001 vs. NASH PEG ^p < .05 vs. NASH OA. (c) Triglyceride (TG) content in primary hepatocytes and HepG2 cells treated with or without palmitic acid (200 μM), OA or OA-NO2 (1 μM) for 20 h. #p < .05 vs. palmitic acid (n = 3). (b) TG biosynthetic rate determined using [3H]-acetate incorporation into TG in HepG2 cells treated with either OA or OA-NO2 (1 μM) for 6 h (n = 3). #p < .05 vs. vehicle control (EtOH).