淫羊藿素抑制人脐静脉内皮细胞血管生成及其机制

摘要

目的：探讨淫羊藿素对人脐静脉内皮细胞（ HUVEC）血管生成的抑制作用及其机制。方法：体外培养人脐静脉内皮细胞，分别观察淫羊藿素对其增殖、迁移及其小管形成的影响。采用酶联免疫吸附法检测血管内皮细胞生长因子（ VEGF ）和色素上皮衍生因子（ PEDF）的含量。结果：经淫羊藿素作用48 h后，未见对内皮细胞增殖有影响。淫羊藿素高浓度组（ ICT110-6 mol/L）、中浓度组（ICT210-7 mol/L）、低浓度组（ICT310-8 mol/L）和沙利度胺（TLD）组HUVEC细胞迁移数目（4.67±1.26）、（10.48±3.15）、（21.06±6.83）和（19.15±6.03）个，明显低于空白对照（Control）组（41.38±7.78）个（P＜0.01）。 ICT1、ICT2、ICT3及TLD组小管形成的面积分别为（5867.45±925.36）、（1627.33±288.56）、（735.73±325.65）和（2933.24±741.43）μm2/视野，均低于Control组（7883.69±1034.85）μm2/视野（P＜0.01）。经淫羊藿素处理后，HUVEC细胞分泌VEGF功能明显下降，而分泌PEDF功能明显升高。结论：体外实验结果表明淫羊藿素具有抑制HUVEC细胞血管生成的作用，这种效应与血管内皮细胞VEGF的活性降低及其合成受到抑制，同时对PEDF活性升高及其合成受到促进作用有关。%Objective:To investigate the suppressive effect of Icaritin on angiogenesis of human umbilical vein endothelial cells ( HU-VEC) and its associated mechanisms.Methods:HUVEC cells were cultured in vitro, and we observed the effects of Icaritin on its prolif-eration, migration and tube formation .The content of vascular endothelial growth factor ( VEGF) and pigment epithelium-derived factor (PEDF) was detected by ELISA.Results:Icaritin had no significant effect on the proliferation of HUVEC cells after 48h treatment.The number of migrated cells in Icaritin high concentration group ( ICT1 10 -6 mol/l) , middle concentration group ( ICT2 10 -7 mol/l) , low concentration group (ICT3 10 -8 mol/l) and Thalidomide (TLD) group were 4.67 ±1.26, 10.48 ±3.15, 21.06 ±6.83, 19.15 ±6.03 respectively, and all of which were lower compared with the control group (41.38 ±7.78) (P<0.01).The area of tube formation in ICT1、ICT2、ICT3 and TLD were separately 5 867.45 ±925.36, 1 627.33 ±288.56, 735.73 ±325.65, 2 933.24 ±741.43μm2 per vi-sion, all of which were lower than the control group (7 883.69 ±1 034.85 μm2 per vision) (P<0.01).After Icaritin treatment, HU-VEC cells had a significant lower ability to secret VEGF , but asfor PEDF , it was on the opposite situation .Conclusion:Icaritin can in-hibit the angiogenesis of HUVEC cells in vitro .Such effect may be related to the decreased activity and synthesis of VEGF in vascular en -dothelial cells , and also associated with the increased activity and synthesis of PEDF .