ABSTRACT
Objective: To investigate the effects of oxymatrine(OM) on the apoptosis of human hepatoma HepG2 cells and its possible mechanisms. Methods: HepG2 cells were treated with different concentrations of OM. The proliferation inhibition was measured by MTT assay and the apoptosis of HepG2 cells were examined by Hochest staining method. Flow cytometry was used to analyze the cell cycle distribution and apoptosis rate. The expression of caspase-3, Bcl-2, Bcl-xL and Bax proteins was assayed by Western blotting assay. Results: OM inhibited HepG2 cells growth in a time- and dose-dependent manner. After treatment with OM for 24 hours, some cells appeared typical apoptotic characteristics and the apoptosis rate was increased. Treatment with OM also increased caspase-3 activity and Bax expression in HepG2 cells, and decreased the expression levels of Bcl-2 and Bcl-xL. Conclusion: OM can induce HepG2 cell apoptosis, which may be related to the down-regulation of PI3K/Akt signal pathway, suppression of Bcl-2 and Bcl-xL activity, and activation of caspase-3.
ABSTRACT
Objective:To investigate the effects of oxymatrine(OM)on the apoptosis of human hepatoma HepG2 cells and its possible mechanisms.Methods:HepG2 cells were treated with different concentrations of OM.The proliferation inhibition was measured by MTT assay and the apoptosis of HepG2 cells were examined by Hochest staining method.Flow cytometry was used to analyze the cell cycle distribution and apoptosis rate.The expression of caspase-3,Bcl-2,Bcl-x_L and Bax proteins was assayed by Western blotting assay.Results:OM inhibited HepG2 cells growth in a time-and dose-dependent manner.After treatment with OM for 24 hours,some cells appeared typical apoptotic characteristics and the apoptosis rate was increased. Treatment with OM also increased caspase-3 activity and Bax expression in HepG2 cells,and decreased the expression levels of Bcl-2 and Bcl-x_L.Conclusion:OM can induce HepG2 cell apoptosis,which may be related to the down-regulation of PI3K/Akt signal pathway,suppression of Bcl-2 and Bcl-x_L activity,and activation of caspase-3.