Cytotoxic effects of procyanidins from Castanea mollissima Bl. shell on human hepatoma G2 cells in vitro

- CSPC inhibits HepG2 cell proliferation in a dose-dependent manner (100-400 μg/mL).
- HepG2 cell cycle is arrested by CSPC in the G0/G1 phase.
- CSPC can induce apoptosis and trigger necrosis of HepG2 cell.
- CSPC causes a loss of mitochondrial membrane potential in HepG2 cell.
- CSPC stimulates reactive oxidative species generation in HepG2 cell.

Significant cytotoxic effects of procynadins from chestnut (Castanea mollissima Bl.) shell (CSPC) on human hepatoma G2 (HepG2) cells were found in vitro. CSPC could inbibit HepG2 proliferation in a dose-dependent manner (100-400 μg/mL), arrest cell cycle in the G0/G1 phase, induce apoptosis and trigger necrosis of HepG2. Proapoptotic effect of CSPC was evidenced by nuclear condensation, internucleosomal DNA fragmentation. Treatment of HepG2 cells with CSPC caused a loss of mitochondrial membrane potential and stimulated reactive oxidative species (ROS) generation. These results suggested CSPC could trigger apoptosis and necrotic cell death in HepG2 cell, which might be associated with ROS generation through the mitochondria-dependent signaling way.