同型半胱氨酸对血管生成的影响及叶酸的作用

Homoeysteine effects on angiogenesis and the role of folic acid

目的通过研究不同浓度同型半胱氨酸（homocysteine，HCY）对人脐静脉内皮细胞血管生成的影响及叶酸（folicacid，FA）对其的保护作用。方法实验分6组，0、1、10、100μmol／L同型半胱氨酸，10μmol／L同型半胱氨酸＋100μmol／L叶酸，100μmol／L叶酸，进行体外血管生成能力实验，Transwell迁移能力检测。Western-blot检查血管生成及迁移相关蛋白表达。结果同型半胱氨酸能明显抑制血管生长因子的表达，降低人脐静脉内皮细胞的成血管环能力。同型半胱氨酸能明显抑制迁移相关蛋白表达，降低人脐静脉内皮细胞的迁移运动能力。叶酸能改善同型半胱氨酸的抑制作用。结论同型半胱氨酸通过抑制血管生长因子、ROCKl／2的表达，从而抑制血管内皮细胞分裂增殖、血管环生成及迁移能力，导致内皮功能障碍，而叶酸能改善这种抑制作用。

Objective To investigate the protective effects of folic acid（FA） on homocysteine （HCY）-induced angiogenesis activity in human umbilical vein endothelial cells（HUVECs）. Methods HUVECs were divided into six groups： treatment groups（0, 1,10,and 100 μmol/L） HCY and FA pre- treatment groups（FA 100 μmol/L）,and HCY 10μmol/L＋ FA 100 μmol/L. HUVECs in vitro anglo- genesis kit, and migration were assayed by transwell kit. The VEGF, VEGFR2, ROCK1, ROCK2, MMP9 protein expression were measured by Western-blot analysis. Results HCY does-dependently impaired the in vitro angiogenesis and migration capacity of HUVECs, because of HCY caused a signif- icant downregulation of VEGF, ROCK1, ROCK2 protein expression. These effects of HCY on HU- VECs were reversed by FA. Conclusions Homocysteine-induced dysfunction in Endothelial dysfunc- tion（ED）, which may be casued by HCY effects on downregulation of VEGF, ROCK1, ROCK2 protein expression,impaired the proliferation, and in vitro Angiogenesis capacity of HUVECs, while FA can improve this inhibition.