Glabridin Mediate Caspases Activation and Induces Apoptosis through JNK1/2 and p38 MAPK Pathway in Human Promyelocytic Leukemia Cells
Figure 3
Activation of caspase 3, -8, -9 and PARP were increased in Glabridin-treated HL-60 cells.
(A) HL-60 cells were treated with 10, 20 and 40 µM glabridin for 24 h and subjected to western blotting with an antibody against PARP or caspase-3, -8 and -9 antibody. (B) The values under each lane indicate relative density of the band normalized to α-tubulin using a densitometer. Values represent the mean ± SE of three independent experiments. (*, #, &, $) p<0.05 compared to the vehicle control groups. (C) HL-60 cells were treated with 40 µM glabridin for 2, 4, 8 and 24 h, subjected to western blotting with an antibody against caspase-3, -8 and -9 antibody. (D) The values under each lane indicate relative density of the band normalized to β-actin using a densitometer. Values represent the mean ± SE of three independent experiments. (*, #, &) p<0.05 compared to the vehicle control groups. (E) HL-60 cells were treated with 10, 20 and 40 µM glabridin for 24 h and subjected to western blotting with an antibody against Bid, Bax, Bad and Bcl-2 antibody. (F) The values under each lane indicate relative density of the band normalized to α-tubulin using a densitometer. Values represent the mean ± SE of three independent experiments. (*, #, &, $) p<0.05 compared to the vehicle control groups.