二氢青蒿素抑制K562细胞血管内皮生长因子的表达

目的通过观察二氢青蒿素抑制K562细胞血管内皮生长因子(VEGF)的表达，探讨青蒿素类药物在抑制血液肿瘤血管新生方面的作用。方法运用MTT法、免疫组化分析和Western blotting分析等探讨了二氢青蒿素对K562细胞增殖以及VEGF表达方面的影响，并进一步对药物预处理后肿瘤细胞的条件培养基在促内皮细胞增殖以及促鸡胚绒毛尿囊膜(CAM)血管新生的作用进行评定。结果二氢青蒿素能有效抑制K562细胞的增殖，并显著下调K562细胞VEGF蛋白和mRNA的表达。同时,药物预处理细胞的条件培养基，其促内皮细胞增殖和促CAM血管新生的能力都有所下降，并呈药物浓度依赖性。结论二氢青蒿素能显著下调K562细胞VEGF的表达，并能抑制由其诱导的血管新生作用。

Dihydroartemisinin inhibits the expression of vascular endothelial growth factor in K562 cells

AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: DHA could effectively downregulate the VEGF expression in K562 cells, and inhibit the leukemic angiogenesis induced by K562 cells.