| 维生素E抑制同型半胱氨酸介导的血管平滑肌细胞增殖 |
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| 引用本文： | 邹彤,刘楠,李树德,苏永春,满勇,陆地. 维生素E抑制同型半胱氨酸介导的血管平滑肌细胞增殖[J]. 南方医科大学学报, 2007, 27(6): 783-786 |
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| 作者姓名： | 邹彤 刘楠 李树德 苏永春 满勇 陆地 |
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| 作者单位： | 北京医院,心内科,北京,100031;北京医院,检验科,北京,100031;昆明医学院,基础医学院,云南,昆明,650031;南方医科大学生物医学工程学院,广东,广州,510515;卫生部老年病研究所,北京,100031;昆明医学院,生物医学工程研究中心康复工程研究室,云南,昆明,650031 |
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| 基金项目： | 国家自然科学基金 , 广东省自然科学基金 |
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| 摘 要： | 目的 探讨在同型半胱氨酸诱导的血管平滑肌细胞(VSMC)增殖中,活性氧(ROS)的作用和维生素E的影响.方法 [3H]-胸腺嘧啶脱氧核苷掺人法测定细胞DNA合成率,锥虫蓝染色计数细胞数量,DCF-DA荧光探针测定细胞内ROS.结果 (1)同型半胱氨酸诱导VSMC的DNA合成增加,促进细胞增殖和ROS水平升高;尽管半胱氨酸诱导VSMC内ROS水平升高,但是对细胞DNA合成和增殖无影响.(2)过氧化氢酶抑制同型半胱氨酸介导的VSMC内ROS升高,而对VSMC增殖无影响.(3)α-生育酚、β-生育酚均可抑制同型半胱氨酸诱导VSNC内ROS水平升高,但是只有α-生育酚显著抑制VSMC增殖.结论 ROS升高不是同型半胱氨酸诱导的VSMC增殖的原因之一.维生素E降低同型半胱氨酸诱导的VSMC增殖可能与抑制蛋白激酶C活性有关,而与它的抗氧化性无关.
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| 关 键 词： | 同型半胱氨酸 血管平滑肌细胞 细胞增殖 维生素E 活性氧物质 |
| 文章编号： | 1673-4254（2007）06-0783-04 |
| 修稿时间： | 2006-10-26 |
Vitamin E inhibits homocysteine-mediated smooth muscle cell proliferation |
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| ZOU Tong,LIU Nan,LI Shu-de,SU Yong-chun,MAN Yong,LU Di. Vitamin E inhibits homocysteine-mediated smooth muscle cell proliferation[J]. Journal of Southern Medical University, 2007, 27(6): 783-786 |
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| Authors: | ZOU Tong LIU Nan LI Shu-de SU Yong-chun MAN Yong LU Di |
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| Affiliation: | 1 Department of Cardiology, 2 Department of Clinical Laboratory, Beijing Hospital, Beijing 100031, China; 3 Faculty of Basic Medicine, 6 Rehabilitation Engineering Research Laboratory, Biomedicine Engineering Research Center, Kunming Medical College, Kunming 650031, China; 4 School of Biomedical Engineering, Southern Medical University, Guangzhou 510515; 5 Institute of Geriatrics, Beijing 100730, China |
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| Abstract: | OBJECTIVE: To investigate the role of reactive oxygen species (ROS) and the effect of vitamin E on proliferation of vascular smooth muscle cells (VSMCs) induced by homocysteine. METHODS: DNA synthesis in the VSMCs cells was measured using [3H]-thymidine incorporation assay, and the cell number determined by trypan blue method. The level of ROS in the cells was determined using DCF-DA as the fluorescence probe. RESULTS: Homocysteine promoted VSMC DNA synthesis, proliferation, and ROS production. Cysteine resulted in increased ROS production in VSMCs, but had no significant effect on DNA synthesis and cell proliferation. Catalase significantly inhibited ROS production induced by homocysteine, but did not significantly inhibited homocysteine-mediated proliferation of VSMCs. While alpha-tocopherol and beta-tocopherol both suppressed increased ROS production induced by homocysteine in VSMCs, only alpha-tocopherol significantly inhibited homocysteine-mediated VSMC proliferation. CONCLUSION: ROS is not associated with VSMC proliferation, and vitamin E-induced suppression of VSMC proliferation is probably related to protein kinase C inhibition. |
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| Keywords: | homocysteine vascular smooth muscle cells cell proliferation vitamin E reactive oxygen species |
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