Figure 1. Urolithin A (UroA) suppressed HepG2.2.15 cell proliferation via caspase-3 dependent apoptosis. A, HepG2.2.15 cells were administrated with 0–120 µM of urolithin A for 24 or 48 h. Cell viability was assessed by a CCK assay and the data were normalized to normal controls. B, The caspase-3 inhibitor Z-DEVD-FMK alleviated urolithin A-induced HepG2.2.15 cell death (80 or 120 µM). The cells were incubated in the absence or presence of Z-DEVD-FMK (20 µM) for 6 h prior to urolithin A treatment, and then incubated for 48 h. Data are reported as means±SD, n=3. ^a,bP<0.05 vs 80 or 120 µM of urolithin A group. C, and D, After urolithin A (80 µM) administration for 48 h, western blot analysis for the protein expressions of cleaved caspase-3, Bcl-2, and Bax was performed in the absence or presence of Z-DEVD-FMK. Data are reported as means±SD, n=3. *P<0.05 compared to the 80 µM urolithin A group (t-test).