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| 同型半胱氨酸诱导人脐静脉血管内皮细胞活性氧升高的机制研究 | |
| 引用本文： | 杨红玲,张敏,甘萍,田兴亚,单妍,李树德. 同型半胱氨酸诱导人脐静脉血管内皮细胞活性氧升高的机制研究[J]. 昆明医学院学报, 2009, 30(6): 19-22 |
| 作者姓名： | 杨红玲 张敏 甘萍 田兴亚 单妍 李树德 |
| 作者单位： | 1. 云南省第三人民医院心内科,云南昆明,650011 2. 昆明医学院第一附属医院心内科,云南昆明,650032 3. 昆明医学院海源学院生物化学教研室,云南昆明,650031 4. 昆明医学院生物化学教研室,云南昆明,650031 |
| 基金项目： | 国家自然科学基金，昆明医学院海源学院科研基金 |
| 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． |
| 关 键 词： | 同型半胱氨酸 血管内皮细胞 活性氧物质 抗氧化酶 增殖 |
The Mechanisim Underlying Enhancement of ROS Production in Vascular Endothelial Cells Induced by Homocysteine |
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| YANG Hong-ling,ZHANG Min,GAN Ping,TIAN Xing-ya,SHAN Yan,LI Shu-de. The Mechanisim Underlying Enhancement of ROS Production in Vascular Endothelial Cells Induced by Homocysteine[J]. Journal of Kunming Medical College, 2009, 30(6): 19-22 | |
| Authors: | YANG Hong-ling ZHANG Min GAN Ping TIAN Xing-ya SHAN Yan LI Shu-de |
| Affiliation: | YANG Hong - ling , ZHANG Min, GAN Ping, TIAN Xing - ya , SHAN Yan , LI Shu - de (1) Dept. of Cardiology, The 3rd People＇s Hospital of Yunnan, Kunming Yunnan 650011; 2 ) Dept. of Cardiology, The 1st Affiliated Hospital, Kunming Medical University, Kunming Yunnan 650032; 3 ) Dept. of Biochemistry, School of Hai Yuan, Kuaming Medical University, Kunming 650031 ; 4 ) Dept. of Biochemistry, Kunming Medical University, Kunming Yunnan 650031, China) |
| Abstract: | 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. |
| Keywords: | Homocysteine Vascular endothelial cell Reactive oxygen species Antixoidant enzyme Proliferation |
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