Figure 3.

Inhibition of TrxR induces apoptosis in liver cancer in a ROS-dependent manner. HepG2 and Hepa1-6 cells were treated with different concentrations of AA1 for 6 h. Accumulation of ROS in the cells was evaluated following DCFH-DA staining. Images were acquired by fluorescence microscopy (scale bar, 10 µm for HepG2 cells and 20 µm for Hepa1-6 cells) (A) HepG2 and Hepa1-6 cells were either treated with AA1, pretreated with NAC followed by AA1 treatment, or treated with NAC alone for the designated periods of time. (B) Levels of p-p38-MAPK, p-JNK and p-ERK levels were examined by western blotting. (C) HepG2 and Hepa1-6 cells either pre-treated with NAC or untreated were subsequently treated with AA1 for 12 h. The percentage of cells undergoing apoptosis was detected by flow cytometry using an Annexin V/propidium iodide assay. Data are expressed as the mean ± standard deviation from at least three independent experiments. *P<0.05: AA1-treated group vs. the untreated group (0 µM); ^#P<0.05: AA1+NAC vs. AA1-treated group. p-ERK, phosphorylated-extracellular signal regulated kinase; JNK, mitogen-activated protein kinase 8; MAPK, mitogen-activated protein kinase; NAC, N-acetylcysteine; AA1, chloro(triethylphosphine)gold(I).