诊断学理论与实践 ›› 2017, Vol. 16 ›› Issue (05): 504-509.doi: 10.16150/j.1671-2870.2017.05.010

• 论著 • 上一篇    下一篇

Toll样受体4参与调控脂质诱导的平滑肌细胞炎症反应的研究

王燕萍1,2, 陈媛媛1,2, 吴丽苹1,2, 陈亚芬1,2, 杨克1, 刘艳1,3   

  1. 1.上海交通大学医学院 心血管病研究所,上海 200025;
    2.上海交通大学医学院附属瑞金医院心内科,上海 200025;
    3.上海交通大学医学院附属第九人民医院心内科,上海 200011
  • 收稿日期:2017-06-20 出版日期:2017-10-25 发布日期:2017-10-25
  • 通讯作者: 刘艳 E-mail: liuyan_ivy@126.com
  • 基金资助:
    国家自然科学基金(81470547); 上海市科委自然科学基金(15ZR1426100)

Toll-like receptor 4 regulates the inflammation induced by lipids in smooth muscle cells

WANG Yanping1,2, CHEN Yuanyuan1,2, WU Liping1,2, CHEN Yafen1,2, YANG Ke1, LIU Yan1,3   

  1. 1. Institute of Cardiovascular Disease, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China;
    2. Department of Cardiology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China;
    3. Department of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
  • Received:2017-06-20 Online:2017-10-25 Published:2017-10-25

摘要: 目的:探究Toll样受体4(Toll-like receptor 4 , TLR4)调控脂质诱导平滑肌炎症反应的机制。方法:使用TLR4敲除小鼠(以野生型C57BL/6小鼠为对照),随机分组为对照组(普通饲料)和实验组(高脂饲料喂养),每组各6只,12周后观察动脉斑块进展情况。体外培养TLR4基因敲除小鼠(以野生型C57BL/6小鼠为对照)的原代平滑肌细胞。此外,使用TLR4特异性抗体阻断TLR4活性后,观察氧化型低密度脂蛋白(oxidized low density lipoprotein,oxLDL)刺激下炎症因子反应。结果:高脂喂养可显著促进野生型小鼠主动脉平滑肌细胞炎症因子表达,而高脂喂养TLR4基因敲除小鼠平滑肌细胞中炎症因子表达水平无明显升高;TLR4特异性抗体可抑制oxLDL诱导的炎症反应。结论:Toll样受体4通过上调平滑肌细胞中炎症因子水平参与oxLDL诱导的炎症反应。

关键词: Toll样受体4, 平滑肌细胞, 脂质, 炎症反应, 炎症因子

Abstract: Objective: To investigate the mechanism of TLR4 in mediating the oxLDL-induced inflammation in smooth muscle cells (SMCs). Methods: TLR4 knockout mice and wild type C57BL/6 mice were randomly divided into control group (normal diet) and study group (high-fat diet) with 6 mice per group. Progression of atheroma was analyzed after 12 weeks in TLR4 knockout mice and wild type C57BL/6 mice. Primary SMCs of TLR4 knockout mice were cultured in vitro, and SMCs of wild type C57BL/6 were served as controls. SMCs were treated with oxLDL to induce inflammation, then TLR4 antibody was used to block TLR4 activity, and oxLDL-induced inflammation was compared between TLR4 knockout mice and wild type C57BL/6 mice. Results: High-fat diet could promote the expression of inflammatory cytokines in wild type C57BL/6 mice, but in TLR4 knockout mice there was no significant difference between the normal and high-fat diet groups. Moreover, blocking the activity of TLR4 could inhibit the oxLDL-induced inflammation in primary SMCs. Conclusions: TLR4 plays a role in regulating the oxLDL-induced inflammation in SMCs.

Key words: Toll-Like Receptor 4, Smooth Muscle Cells, Lipid, Inflammation, Cytokines

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