Figure 7
From: Anti-cancer potential of persimmon (Diospyros kaki) leaves via the PDGFR-Rac-JNK pathway

The effects of EEDK on cell death are dependent on JNK-AP-1/p53 activity. (a,b) Viability of (a) HEK293A and (b) HepG2 cells treated with or without the control (0.5% (v/v) DMSO), EEDK (100 μg/mL), anisomycin (JNK activator, 4 μM), CoCl2 (hypoxia mimicking agent, 150 μM), and T-5224 (AP-1 inhibitor, 10 μM) for 24 h, as measured using the viability assay (n = 4). (c,d) Viability of (c) HEK293A and (d) HepG2 cells treated with or without the control (0.5% (v/v) DMSO), EEDK (100 μg/mL), and pepstatin A (aspartic proteases inhibitor, 1 μM) for 24 h, as measured using the viability assay (n = 3). Anisomycin was used as a positive control. Pepstatin A is a known suppressor of p53 and TNF-α induced apoptosis. The bar graphs present the mean values of cell viability, with error bars indicating the S.E.M (*P < 0.05, **P < 0.01, ***P < 0.001 and #P < 0.0001, Student’s t-test).