Fig. 4

Effect of SEE, and FSEE on caspase-dependent apoptosis by activating the mitochondrial apoptotic pathways in HepG2 cells. Cells were pretreated with 10 μM z-vad-fmk for 2 h, and then incubated with 300 μg/mL of SEE, and 200–300 μg/mL of FSEE for 24 h. Effects of the caspase inhibitor on (a) SEE, and FSEE-induced morphological changes, and (b) cell death in HepG2 cells were examined. After 24 h treatment, (c) total cell lysates were subjected to detect expression of apoptosis-related proteins in HepG2 cells. Data values were expressed as mean ± SD of triplicate determinations. Significant differences were compared with control at *p < 0.05, **p < 0.01, and ***p < 0.001 using one-way ANOVA