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. 2023 May 8;15(9):2232. doi: 10.3390/nu15092232

Figure 4.

Figure 4

Both PE- and TGF-β-induced histone H3K9 acetylation pathways were blocked by 6-shogaol treatment. Cardiomyocytes and cardiac fibroblasts were treated with 6-shogaol (0.3 or 1 μM), followed by stimulation with 30 μM PE for 48 h or 10 ng/mL TGF-β for 6 h, respectively. (A,C) Histone fractions isolated from cardiomyocytes, and cardiac fibroblasts were subjected to Western blotting using anti-acetyl-histone H3 (Lys9) antibodies and anti-histone H3 antibodies. (B,D) Acetylated histone H3K9 and total histone H3 levels were quantified. Data are shown as the mean ± SEM of three (cardiomyocyte) and four (cardiac fibroblast) experiments. (E,F) A p300-HAT domain fragment (residues 1284–1674) was used to perform in vitro HAT assays with 6-shogaol (0.01–100 μM) or 1% DMSO as a control. (E) All samples were subjected to Western blotting with anti-acetyl-histone H3 (Lys9) and anti-histone H3 antibodies. (F) A concentration–response curve was generated by plotting acetyl-histone H3K9/histone H3 vs. log [concentrations]. The quantification is shown as the mean ± SEM of four individual experiments.