中文摘要：

目的探讨同型半胱氨酸诱导血管内皮细胞活性氧（ROS）升高的机制．方法用DCF—DA荧光探针测定人脐静脉血管内皮细胞（HUEVC）内ROS；用[3H]胸腺嘧啶脱氧核苷掺入法测定细胞DNA合成率；采用实时定量PCR测定基因的表达．结果同型半胱氨酸诱导HUEVC的ROS水平升高并抑制细胞增殖．抗氧化剂TEMPOL降低同型半胱氨酸对HUEVC增殖的抑制作用．同型半胱氨酸抑制HUEVC的过氧化氢酶和谷胱甘肽氧化还原酶的基因表达．在高同型半胱氨酸血症小鼠胸主动脉中，过氧化氢酶、锰超氧化歧化酶和谷胱甘肽氧化还原酶基因表达均明显降低．结论同型半胱氨酸诱导的ROS产生导致HUEVC增殖抑制．同型半胱氨酸诱导的ROS升高与抗氧化酶基因表达下调有关．

英文摘要：

Objective To investigate the mechanism underlying the enhancement of homocysteine-indueed production of reactive oxygen species （ROS） in vascular endothelial cells. Methods The levels of ROS in cells were measured by using DCF-DA as a fluorescence probe; DNA synthesis in cells was determined by using [3H] -thymidine incorporation. The expression of tested genes was detected by real-time PCR. Results Homocysteine promoted the levels of ROS and inhibited proliferation in HUEVC. Antioxidant TEMPOL suppressed the inhibitory effect of homoeysteine on proliferation in HUEVC. Homocysteine down-regulated the expression of catalase and glutathione peroxidase. The expression of catalase, glutathione peroxidase, and Mn-SOD decreased in aorta of mice with hyperhomocysteinemia. Conclusion ROS induced by homocysteine inhibit the proliferation of HUEVC. The increase in ROS production induced by homocysteine is due to down-regulation of the expression of antioxidant genes.