Li Jun, Zhou Hui-jun
Department of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310031, China.
Yao Xue Xue Bao. 2005 Nov;40(11):1041-5.
To 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.
Firstly, 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.
DHA 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.
DHA could effectively downregulate the VEGF expression in K562 cells, and inhibit the leukemic angiogenesis induced by K562 cells.
研究双氢青蒿素（DHA）对K562细胞血管内皮生长因子（VEGF）表达的影响，并评估DHA对K562细胞诱导的白血病血管生成的作用。
首先，分析DHA对K562细胞的抗增殖作用，并评估其对K562细胞中VEGF表达的抑制作用。进一步地，评估用DHA预处理的K562细胞的条件培养基（CM）对内皮细胞增殖的刺激作用以及在鸡胚绒毛尿囊膜（CAM）模型上的血管生成作用。
DHA在体外有效抑制K562细胞的增殖，IC50为13.08微摩尔×L（-1）。用DHA处理48小时后，即使在较低浓度（2微摩尔×L（-1））下，K562细胞的VEGF水平也显著降低（P < 0.05）。用DHA预处理的K562细胞的CM对内皮细胞增殖和CAM模型上血管生成 的刺激作用以剂量依赖方式减弱。
DHA可有效下调K562细胞中VEGF的表达，并抑制K562细胞诱导的白血病血管生成。
