上海口腔医学 ›› 2014, Vol. 23 ›› Issue (4): 409-412.

• 基础研究 • 上一篇    下一篇

高脂血症抑制载脂蛋白E基因敲除小鼠对牙龈卟啉单胞菌炎症反应的影响

雷浪1, 李厚轩1, 黄美香1, 陈帅1, 闫福华2   

  1. 1.福建医科大学附属口腔医院·口腔医学院,福建 福州 350002;
    2.南京大学医学院附属口腔医院,江苏 南京 210008
  • 收稿日期:2013-10-22 出版日期:2014-08-20 发布日期:2014-10-20
  • 通讯作者: 闫福华,Tel: 025-83620362,Fax: 025-83620202,E-mail:fhyan2005@126.com
  • 作者简介:雷浪(1979-), 男, 四川人, 博士, 主治医师, E-mail: leilangdental@163.com
  • 基金资助:
    国家自然科学基金(81170973,81100760)

Hyperlipidemia inhibited inflammatory response to Porphyromonas gingivalis in apolipoprotein E knockout mice

LEI Lang1, LI Hou-xuan1, HUANG Mei-xiang1, CHEN Shuai1, YAN Fu-hua2   

  1. 1.School and Hospital of Stomatology, Fujian Medical University. Fuzhou 350002, Fujian Province;
    2.Institute and Hospital of Stomatology, Nanjing University Medical School. Nanjing 210008, Jiangsu Province, China
  • Received:2013-10-22 Online:2014-08-20 Published:2014-10-20
  • Supported by:
    Supported by National Natural Science Foundation of China (81170973 and 81100760).

摘要: 目的:研究高脂血症在ApoE基因敲除(ApoE-/-)小鼠对牙龈卟啉单胞菌(P. gingivalis)炎症反应过程中的影响及其机制。方法:利用ApoE-/-小鼠建立长时间高脂血症模型,腹腔注射活P. gingivalis以建立腹膜炎症模型,倍比稀释法分析腹腔内清除细菌能力,ELISA法检测血液中白细胞介素6(IL-6)和单核细胞趋化因子1(MCP-1)的分泌,实时定量PCR检测腹腔细胞IL-6和MCP-1的转录水平,采用SPSS13.0软件包进行统计学分析。结果:高脂血症显著降低了腹腔清除P. gingivalis的能力,ApoE-/-小鼠腹腔细胞中IL-6和MCP-1转录水平下降,释放入血液中的IL-6和MCP-1水平下降。结论:高脂血症导致宿主对P. gingivalis炎症反应不足,清除细菌能力下降,加速了牙周病的发展进程。

关键词: 高脂血症, 牙龈卟啉单胞菌, 牙周病

Abstract: PURPOSE: To investigate the effect and mechanism of hyperlipidemia on inflammatory response to Porphyromonas gingivalis(P. gingivalis) in apolipoprotein E knock out(ApoE-/-) mice. METHODS: Long term hyperlipidemia model was established in ApoE-/- mice, and viable P. gingivalis were injected into peritoneal cavity to make peritonitis model. Bacteria clearance capability was detected by serial dilution, production of pro-inflammatory cytokine interleukin-6 (IL-6) and monocyte chemotactic protein-1(MCP-1)in serum was measured by ELISA, and IL-6 as well as MCP-1 transcription in peritoneal cells was determined by real time PCR. The data was analyzed with SPSS13.0 software package. RESULTS: Hyperlipidemia disrupted P. gingivalis clearance capability in ApoE-/- mice, accompanied by inhibited IL-6 and MCP-1 transcription in peritoneal cells and decreased IL-6 and MCP-1 release into blood. CONCLUSIONS: Hyperlipidemia disrupts inflammatory response to P. gingivalis, leading to decreased bacteria clearance, which may affect periodontitis progression.

Key words: Hyperlipidemia, Porphyromonas gingivalis, Periodontitis

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