›› 2017, Vol. 37 ›› Issue (5): 449-452.

• 综述 • 上一篇    下一篇

缺氧环境下LPS诱导人牙周膜成纤维细胞炎性损伤的研究进展

俞文伟1,徐艳2,李璐3   

  1. 1. 南京医科大学口腔医学院
    2. 南京医科大学附属口腔医院牙周科
    3. 南京医科大学
  • 收稿日期:2016-11-22 修回日期:2016-12-20 出版日期:2017-05-28 发布日期:2017-05-19
  • 通讯作者: 徐艳 E-mail:yanxu@njmu.edu.cn
  • 基金资助:
    国家自然科学基金;江苏省高等学校大学生创新创业训练计划资助项目;江苏省高校自然科学研究面上项目

Research progress of inflammatory injury in human periodontal ligament cells induced by LPS under hypoxia

  • Received:2016-11-22 Revised:2016-12-20 Online:2017-05-28 Published:2017-05-19

摘要: 内毒素(Lipopolysaccharide, LPS)是牙周炎炎症免疫反应中重要的毒力因子之一,直接或间接地作用于牙周膜成纤维细胞导致其炎性损伤。而牙周膜成纤维细胞因其所处位置的特殊性,长期处于相对缺氧的环境中。所以通过体外模拟牙周膜成纤维细胞发生炎性损伤时的体内环境,有利于阐明缺氧条件下细胞炎性损伤机制。本文就缺氧环境下LPS诱导的人牙周膜成纤维细胞炎性损伤的研究做一系统性回顾。

关键词: 缺氧, 内毒素, 牙周炎

Abstract: Lipopolysaccharide(LPS),which is one of the main virulence factors of periodontitis, results in the inflammatory injury of human periodontal ligament cells (hPDLCs) directly or indirectly. However, hPDLCs reside in a inflamed and hypoxic microenvironment due to their special location. Thus, simulating the inflammatory microenvironment of hPDLCs in vivo will be beneficial to clarifying the mechanism of periodontitis. In this paper, research on the inflammatory injury in hPDLCs induced by LPS under hypoxia will be entensively reviewed.

Key words: hypoxia, LPS, periodontitis

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