为了探讨三氧化二砷(As2O3)对肿瘤血管内皮细胞增殖、迁移、血管形成及其凋亡的机制,采用肝癌HepG2细胞上清诱导人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVEC)成为肿瘤血管内皮细胞(tumor-derived endothelial cells,Td-EC),通过细胞迁移、流式细胞术、血管形成实验检测As2O3对HUVEC与Td-EC增殖、迁移、血管形成及其凋亡的影响。结果显示,在同样条件下与HUVEC相比,As2O3在体外抑制Td-EC增殖、迁移和血管的形成及其促进凋亡的作用显著。结论:As2O3在体外可特异地抑制Td-EC增殖、迁移、血管形成及其凋亡。
To study the mechanism of arsenic trioxide(As2O3) on tumor vascular endothelial cell proliferation,migration,angiogenesis and apoptosis,the cells differentiated into tumor-derived endothelial cells(Td-ECs) by co-culturing with supernatants of HepG2 cells,the anti-effect of As2O3 on Td-ECs and HUVEC was detected with cell migration,flow cytometry,blood vessel formation assay.The results showed that As2O3 effected on Td-EC in vitro promote apoptosis,and inhibited their migration and blood vessel formation,was more significant than under the same conditions over HUVEC.Conclusion is that As2O3 in vitro specifically inhibit Td-EC proliferation,migration,angiogenesis and promote apoptosis.