摘要
This study investigated the effect of arctigenin(ARG) on the induction of apoptosis and the putative pathways of its action in HL-60 and K562 cells.MTT assay was used to detect the cytotoxic effect of ARG in HL-60 and K562 cells.The apoptosis was observed by Hoechst 33258 fluorescence staining and DNA agarose gel electrophoresis.Caspase-3 enzyme activity was measured by caspase-3 enzyme activity detection kit.The expression of related protein was analyzed by Western blotting and the vascular endothelial growth factor(VEGF) level was determined by enzyme-linked immunosorbent assay(ELISA).ARG-treated HL-60 cells and K562 cells exhibited growth inhibition and displayed several features of apoptosis,including DNA fragmentation and DNA laddering by agarose gel electrophoresis.It was observed that poly-(ADP-ribose) polymeras(PARP) were cleaved to smaller molecules and ARG induced upregulation of bax and downregulation of bcl-2 protein expression.However,it had no effect on VEGF levels.Taken together,this study demonstrated that ARG is a potent inducer of apoptosis and this was accompanied by caspase-3 activation and upregulation of bax/bcl-2,which offers a potential mechanism for the apoptosis-inducing activity of ARG.
This study investigated the effect of arctigenin （ARG） on the induction of apoptosis and the putative pathways of its action in HL-60 and K562 cells. MTT assay was used to detect the cytotoxic effect of ARG in HL-60 and K562 cells. The apoptosis was observed by Hoechst 33258 fluorescence staining and DNA agarose gel electrophoresis. Caspase-3 enzyme activity was measured by caspase-3 enzyme activity detection kit. The expression of related protein was analyzed by Western blotting and the vascular endothelial growth factor （VEGF） level was determined by enzyme-linked immunosorbent assay （ELISA）. ARG-treated HL-60 cells and K562 cells exhibited growth inhibition and displayed several features of apoptosis, including DNA fragmentation and DNA laddering by agarose gel electrophoresis. It was observed that poly-（ADP-ribose） polymeras （PARP） were cleaved to smaller molecules and ARG induced upregulation of bax and downregulation of bcl-2 protein expression. However, it had no effect on VEGF levels. Taken together, this study demonstrated that ARG is a potent inducer of apoptosis and this was accompanied by caspase-3 activation and upregulation of bax/bcl-2, which offers a potential mechanism for the apoptosis-inducing activity of ARG.
出处
《药学学报》
CAS
CSCD
北大核心
2008年第5期542-547,共6页
Acta Pharmaceutica Sinica
