基础医学与临床 ›› 2011, Vol. 31 ›› Issue (4): 426-429.

• 研究论文 • 上一篇    下一篇

尿酸抑制人脐静脉内皮细胞合成一氧化氮

王琦1,曾学军1,方卫纲2,陈连凤3,何敛4   

  1. 1. 中国医学科学院 北京协和医学院 北京协和医院
    2. 中国医学科学院北京协和医学院北京协和医院普通内科
    3. 中国医学科学院 北京协和医学院 北京协和医院 心内科
    4. 拜耳医药保健有限公司全球药政事务部
  • 收稿日期:2010-10-27 修回日期:2010-12-06 出版日期:2011-04-05 发布日期:2011-04-08
  • 通讯作者: 曾学军 E-mail:zxjpumch@126.com

Uric Acid Inhibits the Synthesis of Nitric Oxide in Human Umbilical Vein Endothelial Cells

Qi WANG1,Xue-jun ZENG1,Wei-gang FANG1,Lian-feng CHEN2,Lian HE2   

  1. 1. PUMC Hospital, CAMS & PUMC
    2.
  • Received:2010-10-27 Revised:2010-12-06 Online:2011-04-05 Published:2011-04-08
  • Contact: Xue-jun ZENG E-mail:zxjpumch@126.com

摘要: 目的 研究尿酸(UA)对人脐静脉内皮细胞(HUVEC)表达内皮型一氧化氮合酶(eNOS)及分泌一氧化氮(NO)的影响。方法 不同浓度UA(0、0.5、1、1.5及2 mg/L)及50 mg/L ox-LDL(阳性对照)分别作用HUVEC 24、48及72h,用real-time PCR法测定HUVEC eNOS mRNA;Western blot法检测细胞eNOS蛋白;酶法检测上清液NO的含量。结果 UA 0.5 mg/L组eNOS mRNA表达水平明显高于对照组(P<0.05);随着UA浓度升高(1、1.5及2 mg/L组),及其作用时间延长,HUVEC eNOS mRNA及蛋白表达水平及上清液NO分泌量相比对照均明显下降(72h NO2-/NO3- 2 mg/L组与对照组为0.52±0.18与1.00±0.1,P<0.05),且趋势与ox-LDL组相同。结论 0.5 mg/L以上浓度的UA呈浓度及时间依赖性抑制HUVEC eNOS表达及NO合成,提示高浓度的UA可能损伤血管内皮功能。

关键词: 尿酸, 内皮功能, 一氧化氮合成酶, 一氧化氮

Abstract: Objective To investigate the effect of uric acid (UA) on the expression of endothelial nitric oxide synthase (eNOS) and the production of nitric oxide in cultured human umbilical vein endothelial cells (HUVECs). Methods HUVECs were incubated with different concentration of UA (0、5、10、15、20mg/dl) and 50mg/L ox-LDL(as positive control) for 24h、48h and 72h.. Then, eNOS mRNA was detected by real-time PCR. The expression of eNOS protein was observed by western blot. NO in supernatant medium was analyzed by Enzymic method. Results UA 5mg/dl group could increase the expression of eNOS mRNA of HUVECs ,compared with placebo control group(P<0.05). While the concentration of UA increasing and time lasting, the expression of eNOS and the production of NO were decreasing significantly(72h NO2-/NO3- is 0.52±0.18 versus 1.00±0.1 for 2 mg/L versus control, P<0.05), the same with ox-LDL. Conclusion UA inhibited the expression of eNOS and the production of NO of HUVECs in a dose-dependent and time-dependent manner. It suggested that UA can damage the function of endothelial cells and may influence genesis and development of cardiovascular diseases.

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