Cytotoxicity and mechanism of 24-O-acetylcimigenol-3-O-β-D- xylopyranoside on HepG2 cells

OBJECTIVE: To elucidate the cytotoxicity and mechanism of 24-O-acetylcimigenol-3-O-β-D-xylopyranoside on HepG2 cells. METHODS: MTT,AO/EB fluorescence staining observation, flow cytometry and western blot methods were used to study the cytotoxicity, morphological changes, cell cycle distribution and protein expression profile of 24-O-acetylcimigenol-3-O-β- D-xylopyranoside on HepG2 cells. RESULTS: 24-O-acetylcimigenol-3-O-β-D- xylopyranoside inhibited the proliferation of HepG2 cells with IC₅₀ at 13 μmol·L^-1, and induced apoptosis and G₂/M cell cycle arrest. Further study demonstrated that the compound cleavaged PARP, down-regulated the antiapoptotic protein expression of bcl 2, up-regulated the apoptotic protein expression of Bax, decreased the expression of cyclin and cyclin dependent kinase cyclin B and cdc2. CONCLUSION: 24-O-acetylcimigenol-3-O- β-D-xylopyranoside exerts its cytotoxicity on HepG2 cells via apoptosis and G₂/M arrest. In addition, caspases family activation, the down-regulation of bcl2 and the up-regulation of Bax contributed to apoptosis, and the down-regulation of cdc2 and cyclin B are associated with G2/M arrest.