Molecular mechanisms of apoptosis induced by Scorpio water extract in human hepatoma HepG2 cells

Figure 1 Effects of SWE on cell viability (A) and DNA fragmentation (B). A: Cells (1×10⁴) treated with various concentrations of SWE for 24 h; B: Cells (3×10⁶) treated with 2.0 mg/mL SWE for the indicated time periods. ^aP<0.05, ^bP<0.01 vs control.

Figure 2 Role of mitochondrial alterations in SWE-treated HepG2 cells. A: Cells (5×10⁵) treated with 2.0 mg/mL SWE for the indicated time periods; B and C: Cells pretreated for 30 min with 5 μmol/L CsA and then treated with 2.0 mg/mL SWE for 6 h. ^aP<0.05 vs control.

Figure 3 SWE induces the activation of caspase-3 and PARP cleavage in HepG2 cells. A: HepG2 cells (1.5×10⁷) treated with 0-5.0 mg/mL of SWE for 24 h; B and C: HepG2 cells treated with 2.0 mg/mL SWE for the indicated time periods. ^aP<0.05, ^bP<0.01 vs control.

Figure 4 Inhibition of SWE-induced caspase-3 activation (A), PARP cleavage (B) and DNA fragmentation (C) by caspase-3 inhibitor or MPT inhibitor. HepG2 cells were pretreated with Ac-DEVD-CHO (25 μmol/L) for 1 h or CsA (5 μmol/L) for 30 min followed by treatment with 2.0 mg/mL SWE for further 24 h. Lane M: DNA marker, lane 1: control, lane 2: 2.0 mg/mL SWE, lane 3: 2.0 mg/mL SWE with 5 μmol/L CsA, lane 4: 2.0 mg/mL SWE with 25 μmol/L Ac-DEVD-CHO. ^bP<0.01 vs control; ^dP<0.01 vs SWE alone.