Induction of apoptosis of the human leukemia cells by arctigenin and its mechanism of action.
- Author:
Lu WANG
1
;
Feng ZHAO
;
Ke LIU
Author Information
1. School of Pharmacy, Yantai University, Yantai 264005, China.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents, Phytogenic;
isolation & purification;
pharmacology;
Apoptosis;
drug effects;
Arctium;
chemistry;
Caspase 3;
metabolism;
Cell Proliferation;
drug effects;
DNA Fragmentation;
drug effects;
Fruit;
chemistry;
Furans;
isolation & purification;
pharmacology;
HL-60 Cells;
Humans;
K562 Cells;
Lignans;
isolation & purification;
pharmacology;
Plants, Medicinal;
chemistry;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
Vascular Endothelial Growth Factor A;
metabolism;
bcl-2-Associated X Protein;
metabolism
- From:
Acta Pharmaceutica Sinica
2008;43(5):542-547
- CountryChina
- Language:Chinese
-
Abstract:
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.