摘要
目的探讨As2O3联合canstatin蛋白对肿瘤血管内皮细胞(Td-EC)增殖、迁移、血管形成的影响及其凋亡的机制。方法用肝癌HepG2细胞上清诱导人脐静脉内皮细胞(HUVEC)成为Td-EC。As2O3联合canstatin干预Td-EC,通过细胞迁移,流式细胞术,观察血管形成。结果 As2O3、canstatin及联合影响Td-EC迁移细胞数分别为32.60±1.51、26.60±1.14、21.00±1.87,显著低于对照组50.60±2.30(P<0.01),并促进凋亡、抑制管腔形成,以联合应用更显著。结论 As2O3联合canstatin在体外可特异地抑制Td-EC增殖、迁移、血管形成及其凋亡。
Objective To study the effect and the mechanism of As203 combined with recombinant canstatin protein on tumor vascular endothelial cell proliferation, migration, angiogenesis and apoptosis. Methods The cells were induced to differentiate into tumor-derived endothelial cells （Td-ECs） by co-culturing with supernatants of HepG2 cells. The anti-effect of As203 and canstatin on Td-ECs was examined by cell migration, flow cytometry, blood ves- sel formation assay. Results As203, canstatin and the combined all effected on Td-EC in vitro inhibited their mi- gration cells respectively ： 32. 60 __. 1.51,26.60 _ 1.14,21.00 -＋ 1.87, significantly _＋ 2.30 （ P 〈 0. 01 ）, and promoted apoptosis, blood vessel formation. The effect of Conclusions As203 combined with recombinant canstatin protein inhibits Td-EC genesis and promotes apoptosis.
出处
《基础医学与临床》
CSCD
北大核心
2012年第12期1389-1394,共6页
Basic and Clinical Medicine
基金
国家自然科学基金(81060174)
关键词
AS2O3
CANSTATIN
凋亡
迁移
血管形成
Ass 03
canstatin
apoptosis
migration
angiogenesis higher than control group 50. 60 combined was more significant. proliferation, migration, angio-
