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. 2018 Nov 9;19(11):3539. doi: 10.3390/ijms19113539

Figure 6.

Figure 6

Histone deacetylase (HDAC) inhibitors reduce the expression of G6P and PCK1 in HepG2 cells. Cells were treated with VPA ((A,F), 0.1, 1.0, and 10 mmol/L); SAHA ((B,G), 0.1, 1.0, and 10 µmol/L); TSA (C, H, 0.1, 0.3, and 1.0 µmol/L); MS275 ((D,I), 1.0, 10, and 100 µmol/L); and MC1568 ((E,J), 0.1, 1.0, and 10 µmol/L) for 48 h under hyperglycemic conditions. Expression of G6P or PCK1 was quantified by RT-qPCR. Cultivation under hyperglycemic conditions increased the expression of G6P or PCK1, an effect that was attenuated by treatment with the pan-HDAC inhibitors VPA, SAHA, and TSA, as well as the HDAC class I-specific inhibitor, MS275, and the HDAC class IIa-specific inhibitor, MC1568. The graphs show the mean ± SEM of three independent experiments (* p < 0.05, ** p < 0.01 vs. vehicle in 30 mmol/L glucose). HDAC inhibitors (VPA, 10 mmol/L; SAHA, 10 µmol/L; TSA, 1.0 µmol/L; MS275, 100 µmol/L; MC1568, 10 µmol/L, for 24 h) also decreased the expression of G6P or PCK1 in the absence of glucose (K,L). The graphs show the mean ± SEM of three independent experiments (* p < 0.05 vs. vehicle in 0 mmol/L glucose).