Figure 2

CGE induced the release of cytochrome-c, activated caspases, and PARP. (A) SKMEL-5 cells were treated with the indicated concentrations of CGE for 48 h, DiOC6 (3) staining was performed, and the mitochondrial membrane potential of the cells were analyzed by flow cytometry. (B) Data are presented as mean ± SD for at least three independent experiments. * P < 0.05 and *** P < 0.001 compared with the control. (C) CGE inhibition caused cytotoxicity by z-VAD FMK, as demonstrated by double staining with annexin V-FITC and PI. (D) Skin cancer cells were exposed to CGE (50 μg·mL^-1) for 8, 24, and 48 h. Cell lysates were prepared and assayed for BAX, Bcl-2, caspase-9, caspase-7, caspase-3, poly-(ADP-ribose)-polymerase (PARP), and GAPDH protein levels. (E) B16F1 and SKMEL-5 cells were treated with 50 μg·mL^-1 CGE for 8, 24, and 48 h. Equal amounts of protein from each sample were separated by SDS-PAGE and immunoblotted with cytochrome-c and GAPDH antibodies.