Antiproliferative effects mechanism of β-sitosterul in hepatoma HepG2 cells

OBJECTIVE To study the antiproliferative effects of beta-sitosterul and its mechanism in hepatoma HepG2 cells. METHOD Cell 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. RESULT beta-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. CONCLUSION beta-Sitosterul exerted antiproliferative effects and induced HepG2 cells apoptosis via mitochondrial pathway and membrane death receptor pathway.