Licochalcone A-Induced Human Bladder Cancer T24 Cells Apoptosis Triggered by Mitochondria Dysfunction and Endoplasmic Reticulum Stress
Figure 4
LCA induced mitochondrial dysfunction, caspase cascade activation, and cleavage of poly(ADP-ribose) polymerase (PARP) in T24 cells. The cells were treated with or without LCA (, and 100 μM) with or without NAC (500 μM). (a) Mitochondrial membrane potential depolarization was determined by flow cytometry. The number of cells with normal polarized mitochondrial membranes (red) and cells with depolarized mitochondrial membranes (green) is expressed as a percentage of total cell number. (b) Caspase-9, caspase-3 expression, and PARP cleavage were examined via western blot analysis (left), and quantitative analysis of caspase-9, caspase-3 and PARP protein levels (right). Control group (LCA-untreated group) level was accepted to be “1.0”. , compared with the LCB-untreated control group; compared with the LCA group alone (50 μM).
