中文摘要：

目的探讨同型半胱氨酸（HCY）对血管内皮细胞核因子-κB（NF-κB）的激活及其机制，以明确HCY在动脉粥样硬化发病过程中的作用。方法从人脐静脉分离血管内皮细胞；用电泳迁移率和免疫荧光方法检测NF-κB的活性；用免疫印迹实验检测κB抑制蛋白（IκB-α）的磷酸化。结果电泳迁移率变动实验（EMSA）证明HCY可以时间依赖性和浓度依赖性地激活血管内皮细胞NF-κB；免疫荧光共聚焦显微镜可见在HCY刺激后的血管内皮细胞，大量的NF-κB-P65蛋白从细胞质转移入细胞核内，故NF-κB-P65蛋白染色在细胞核内呈强阳性，而细胞质内染色较弱；Western blot证明HCY能明显地诱导血管内皮细胞IκB-α的磷酸化。结论HCY可能通过增强IκB-α的磷酸化，抑制血管内皮细胞IκB-α的活性，从而激活NF-κB，在转录水平对下游的趋化因子和黏附因子产生调节作用，促进动脉粥样硬化的形成和发展。

英文摘要：

Objective To understand the activation of NF-κB by homocysteine in vascular endothelial cells and the role of homocysteine during atherogenesis. Methods Vascular endothelial cells were isolated from human umbilical veins, and cultured in M199 medium. The electrophoretic mobility shift assay and immunofluorescent staining were performed to detect the activity of NF-κB. Western blot assay was used to test the phosphorylation of IκB-α. Results Homocysteine inhibited the activity of IκB-α by enhancing the phosphorylation of IκB-α in vascular endothelial cells, and stimulated activation of NF-κB in the cells in a dose- and time-dependent manner. Conclusion Homocysteine activates NF-κB in vascular endothelial cells by inhibiting IκB-α activity, and plays a role in atherogenesis.