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. 2019 Oct 22;9(4):569–585. doi: 10.1016/j.jcmgh.2019.10.005

Figure 6.

Figure 6

Butyrate prevents an ethanol-mediated decrease in recruitment of PGC-1α and p300 to the CPT-1A promoter. Primary hepatocytes were left untreated (UT) or treated with 50 mmol/L ethanol for 12 hours (Ethanol). Cells were pretreated with sodium butyrate (NaB 2 mmol/L) for 30 minutes before ethanol (Ethanol + NaB). ChIP analysis was performed using chromatin fragments immunoprecipitated with (A) anti–PGC-1α and (D) anti-p300 antibodies. ChIP real-time quantitative PCR was performed using primer pairs specific for regions I and II on the CPT-1A promoter. Nonimmunoprecipitated chromatin was used as input. (C and E) Detection of PGC-1α and p300 protein levels by Western blot analysis in mice liver tissues. Blots were stripped and reprobed with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) antibody as a loading control. The density ratio for each band compared with its GAPDH are shown in an adjacent bar graph. (B) PGC-1α mRNA levels were analyzed by real time-qPCR and normalized to β-actin mRNA. Data were analyzed by analysis of variance and represented as means ± SD, n = 4 experiments. P value < .05 (a) when compared with UT and (b) when compared with ethanol.