Figure 6.

Ginsenoside CK inhibited hypoxia induced EMT in vitro. (A) HCC-LM3 cells were treated with ginsenoside CK in the absence or presence of 200 μM CoCl₂ for 24 h. HIF-1α (red), DAPI (blue) immunofluorescence staining, and 2-channel merged images showed the protein expression level and the nuclear translocation of HIF-1α. Magnification 1000×. (B) HepG2 and SMMC-7721 cells were treated with ginsenoside CK in the absence or presence of 200 μM CoCl₂ for 24 h. HIF-1α, EMT related proteins, IκBα and p-IκBα expressions were determined by Western blotting. Quantification plots are shown below. Data were presented as mean ± SD (n = 3). HCC-LM3 cells were treated with ginsenoside CK in the absence or presence of 200 μM CoCl₂ for 24 h. (C) The immunofluorescence staining of p65 (red) and 2-channel merged images showed the nuclear translocation of p65. Magnification 1000×. (D) HIF-1α, EMT related proteins, MMP2, MMP9, IκBα, p-IκBα and nuclear p65 proteins were assessed by Western blot analysis. Quantification plots are shown on the right. Data were presented as mean ± SD (n =3). * p < 0.05, ** p < 0.01 compared with untreated control cells. # p < 0.05, ## p < 0.01 vs. CoCl₂-treated group. The figures shown were representative of three independent experiments.