Antiproliferative effects mechanism of beta-sitosterul in hepatoma HepG2 cells.
- Author:
Zhongquan ZHANG
1
;
Yujun XING
;
Guoqiang HU
;
Songqiang XIE
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; Apoptosis; drug effects; Apoptosis Regulatory Proteins; metabolism; Carcinoma, Hepatocellular; metabolism; pathology; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Hep G2 Cells; Humans; Liver Neoplasms; metabolism; pathology; Membrane Potential, Mitochondrial; drug effects; Sitosterols; pharmacology
- From: China Journal of Chinese Materia Medica 2011;36(15):2145-2148
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the antiproliferative effects of beta-sitosterul and its mechanism in hepatoma HepG2 cells.
METHODCell proliferation was assessed by MTT assay. Cell cycle distribution, apoptosis and mitochondrial membrane potential were measured by high content screening (HCS). The protein expression of caspase-3, caspase-8, caspase-9, Bcl-2, Bax, tBid and cytochrome c in the HepG2 cells were evaluated by Western Blots.
RESULTbeta-Sitosterul exerted significant antiproliferative effects in HepG2 cells. Furthermore, beta-sitosterul also induced HepG2 cells apoptosis, lost mitochondrial membrane potential, activated caspase-3, caspase-8 and caspase-9, up-regulate Bax, tBid protein, down-regulation Bcl-2 protein. However, beta-sitosterul had hardly any effects on QSG7701 cells.
CONCLUSIONbeta-Sitosterul exerted antiproliferative effects and induced HepG2 cells apoptosis via mitochondrial pathway and membrane death receptor pathway.
