血凝素样氧化型低密度脂蛋白受体1介导氧化型低密度脂蛋白促进血管平滑肌细胞表达白细胞介素6
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Oxidized Low Density Lipoprotein Enhances Interleukin-6 Expression of Vascular Smooth Muscle Cell via Lectin-like Low Density Lipoprotein Receptor-1
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    摘要:

    观察氧化型低密度脂蛋白对血管平滑肌细胞白细胞介素6表达的影响及血凝素样氧化型低密度脂蛋白受体1在其中的作用。人脐带动脉平滑肌细胞体外原代培养,传至4~5代。氧化型低密度脂蛋白干预,观察不同时间点白细胞介素6mRNA表达,及不同浓度氧化型低密度脂蛋白对白细胞介素6和血凝素样氧化型低密度脂蛋白受体1mRNA表达的影响。并观察血凝素样氧化型低密度脂蛋白受体1抑制剂多聚肌酐酸对白细胞介素6mRNA表达的影响。结果发现,(1)氧化型低密度脂蛋白作用后,白细胞介素6mRNA表达显著升高,作用6h出现峰值。随着氧化型低密度脂蛋白浓度升高,白细胞介素6mRNA和血凝素样氧化型低密度脂蛋白受体1mRNA表达均明显升高,后两者呈正相关(r=0 .94 3,P<0 .0 1)。(2 )多聚肌酐酸抑制血凝素样氧化型低密度脂蛋白受体1后,白细胞介素6mRNA表达明显下降。以上表明氧化型低密度脂蛋白明显促进血管平滑肌细胞白细胞介素6的表达,血凝素样氧化型低密度脂蛋白受体1在此过程中起重要介导作用。

    Abstract:

    Aim Atherosclerosis is a kind of chronic inflammation. The purpose of this study is to observe, in the inflammation course, how oxidized low density lipoprotein (ox-LDL) impact interleukin-6 (IL-6) expression of vascular smooth muscle cell (VSMC) and how lectin-like low density lipoprotein receptor-1(LOX-1) act as. Methods Smooth muscle cell from human umbilical artery was cultured in vitro. Took 4-5th generation for use. Grouping according to different ox-LDL concentrations and reaction times. Then, detection the quantity of VSMC IL-6 mRNA and LOX-1 mRNA with RT-PCR. Further more, observe how one inhibitor of LOX-1 named as polyinosinic acid influence the production of VSMC IL-6 mRNA. Results 1. The quantity of VSMC IL-6 mRNA increased highly after co-cultured with ox-LDL (p<0.01 or p<0.001). The peak value was found at about 6th hour. The expression of IL-6 mRNA and LOX-1 mRNA were increased with ox-LDL concentration ascending (p<0.01 or p<0.001). There is a positive relationship between IL-6 mRNA and LOX-1 mRNA (r=0.943,p<0.001). 2.IL-6 mRNA was reduced when LOX-1 was inhibited by polyinosinic acid (p<0.01 or p<0.001). Conclusions ox-LDL can induce increased expression of VSMC LOX-1 mRNA. LOX-1 plays a vital rule in this process.

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魏钧伯,魏盟,蔡绳,张英民.血凝素样氧化型低密度脂蛋白受体1介导氧化型低密度脂蛋白促进血管平滑肌细胞表达白细胞介素6[J].中国动脉硬化杂志,2004,12(2):165~168.

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  • 收稿日期:2003-09-08
  • 最后修改日期:2004-02-01
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