【摘要】 目的 初步研究CBS基因缺陷后高同型半胱氨酸（Hcy）对人脐静脉内皮细胞HUVEC功能的作用及可能的分子机制。方法 培养HUVEC内皮细胞，分别设对照组、Hcy处理组、Hcy+GYY4137组；对照组、CBS基因缺陷组、CBS基因缺陷+GYY4137组；采用CCK-8法检测各组细胞活力及细胞增殖情况；DAPI核染色和caspase-3酶活力测定法检测各组内皮细胞凋亡变化；小管形成实验检测各组内皮细胞功能改变；Western blot法检测增殖相关蛋白PCNA的变化。结果 CBS基因缺陷或Hcy均可抑制内皮细胞增殖并促进细胞凋亡，从而导致内皮细胞功能损伤。相反，H₂S外源供体GYY4137可降低CBS基因缺陷或Hcy导致的内皮细胞凋亡，明显改善内皮细胞功能，促进细胞增殖。结论 CBS基因缺陷可能由于高Hcy水平而抑制内皮细胞增殖、促进细胞凋亡，而导致内皮细胞功能障碍；而H₂S外源供体可能促进高Hcy浓度下内皮细胞增殖从而改善CBS基因缺陷后内皮细胞功能。更多还原

【Abstract】 Objective To investigate the effect of high homocysteine（Hcy） on the function of human umbilical vein endothelial cells（HUVEC） with CBS variant and the possible molecular mechanism. Methods HUVEC cells were cultured and divided into control group, Hcy treatment（or Hcy+GYY4137） group and si-CBS（or si-CBS+GYY4137） group. Cell viability and cell proliferation were detected by CCK-8 assay. DAPI nuclear staining and caspase-3 activity assay were used to evaluate apoptosis of endothelial cells in each group. The changes of endothelial cell function were detected by tubule formation assay. The changes of proliferation-related protein PCNA were detected by Western blot. Results Both CBS variant and increasing Hcy concentrations could inhibit the proliferation of endothelial cells and promote apoptosis, thus leading to endothelial cell function damage. However, H₂S exogenous donor GYY4137 can reduce endothelial cell apoptosis caused by CBS variant or high Hcy levels, significantly improve endothelial cell function and promote cell proliferation. Conclusion High Hcy levels after CBS variant may inhibit endothelial cell proliferation and promote apoptosis, leading to endothelial cell dysfunction. H₂S might significantly promote the proliferation of endothelial cells by reducing the concentration of Hcy, thereby improving the function of endothelial cells after CBS deficiency.更多还原