Dihydroartemisinin inhibits the expression of vascular endothelial growth factor in K562 cells.
- Author:
Jun LI
1
;
Hui-jun ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antineoplastic Agents, Phytogenic; administration & dosage; pharmacology; Artemisinins; administration & dosage; pharmacology; Cell Proliferation; drug effects; Chickens; Chorioallantoic Membrane; blood supply; Dose-Response Relationship, Drug; Down-Regulation; Humans; K562 Cells; metabolism; Neovascularization, Pathologic; RNA, Messenger; biosynthesis; genetics; Sesquiterpenes; administration & dosage; pharmacology; Vascular Endothelial Growth Factor A; biosynthesis; genetics
- From: Acta Pharmaceutica Sinica 2005;40(11):1041-1045
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the effect of dihydroartemisinin (DHA) on vascular endothelial growth factor (VEGF) expression in K562 cells and assess the effect of DHA on leukemic angiogenesis induced by K562 cells.
METHODSFirstly, analyzed the anti-proliferation effect of DHA on K562 cells and assessed the inhibitory effect on expression of VEGF in K562 cells. Further, the conditioned medium (CM) of K562 cells pretreated with DHA was assessed for its stimulating effect on proliferation of endothelial cells and angiogenesis on chicken chorioallantoic membrane (CAM) model.
RESULTSDHA effectively inhibited the proliferation of K562 cells in vitro, and the IC50 was 13.08 micromol x L(-1). The VEGF level of K562 cells was significantly lowered after treated with DHA for 48 h, even at a lower concentration (2 micromol x L(-1), P < 0.05). The stimulating effect on proliferation of endothelial cells and angiogenesis on CAM model were weakened in response to the CM from K562 cells pretreated with DHA in a dose-dependent manner.
CONCLUSIONDHA could effectively downregulate the VEGF expression in K562 cells, and inhibit the leukemic angiogenesis induced by K562 cells.
