Cytotoxicity and mechanism of 23-O-acetylcimigenol-3-O-beta-D-xylopyranoside on HepG2 cells.
- Author:
Zel TIAN
1
;
Jian-Yong SI
;
Si-Bao CHEN
;
Meng-Su YANG
;
Pei-Gen XIAO
;
Er-Xi WU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; CDC2 Protein Kinase; metabolism; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Cimicifuga; chemistry; Cyclin B; metabolism; Glycosides; isolation & purification; pharmacology; Humans; Liver Neoplasms; metabolism; pathology; Plants, Medicinal; chemistry; Poly(ADP-ribose) Polymerases; metabolism; Proto-Oncogene Proteins c-bcl-2; metabolism; Triterpenes; isolation & purification; pharmacology; bcl-2-Associated X Protein; metabolism
- From: China Journal of Chinese Materia Medica 2006;31(21):1818-1821
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo elucidate the cytotoxicity and mechanism of 23-O-acetylcimigenol-3-O-beta-D-xylopyranoside isolated from C. dahurica on HepG2 cells and to find the leading compound for new drug development.
METHODMTT, AO/EB staining observation, flow cytometry and western blot methods were used to study the cytotoxicity, morphological changes, cell cycle distribution and protein expression profile of 23-O-acetylcimigenol-3-O-beta-D-xylopyranoside on HepG2 cells.
RESULT23-O-acetylcimigenol-3-O-beta-D-xylopyranoside could inhibit the proliferation of HepG2 cells with IC50 at 16 micromol x L(-1), and could also induce apoptosis and G2-M cell cycle arrest. Further study demonstrated that the compound could cleavage PARP, regulate protein expression of bcl-2 family and decrease the expression of cdc 2 and cyclin B.
CONCLUSION23-O-acetylcimigenol-3-O-beta-D-xylopyranoside exerts its cytotoxicity on HepG2 cells via apoptosis and G2-M arrest. In addition, caspases family activation, regulation of protein expression of bcl-2 family and down regulation of cdc 2 and cyclin B were involved in apoptosis and G2-M arrest induced by it.
