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. 2018 Oct 12;19(10):3127. doi: 10.3390/ijms19103127

Figure 6.

Figure 6

Decreased intracellular cholesterol level by emodin causes the suppression of the oncogenic protein kinase B (AKT) signaling pathway. (A) Simvastatin suppressed the AKT signaling pathways. SK-HEP-1 cells were incubated with different concentrations of simvastatin (2, 5, 10, and 20 μM) for 12 h. (B) Emodin suppressed the phosphorylation of AKT and its target substrates. SK-HEP-1 cells were incubated with emodin (2, 5, 10, and 20 μM) for 12 h. (C) The supplementation of water-soluble cholesterol rescued the decreased phosphorylation of AKT caused by emodin. SK-HEP-1 and HepG2 cells were incubated in the presence or absence of 0.5 mM cholesterol for 1 h prior to emodin treatment. Subsequently, the cells were incubated for a further 12 h, and protein expression was measured by Western blotting.