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相关实验视频

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SIRT3淘汰会加剧LPS诱导的欧斯塔希管功能障碍.

Shimin Zong1,2,3, Huimin Zhang1,2,3, Ting Li1,2,3

  • 1Department of Otorhinolaryngology-Head and Neck Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

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概括

缺少SIRT3的小鼠在暴露于LPS后显示尤斯塔希管功能障碍 (ETD) 恶化,这表明SIRT3对于维持ET功能至关重要,并且可能是中耳炎的治疗点.

关键词:
在LPS中使用LPS.在 MUC5ACAC 中.这就是Sirt3的意思.尤斯塔希安管的功能障碍

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科学领域:

  • 耳鼻喉科 耳鼻喉科 耳鼻喉科
  • 分子生物学分子生物学
  • 免疫学 免疫学 免疫学

背景情况:

  • 急性中耳炎 (AOM) 在儿童中很常见,常常是由阴性细菌引起的.
  • 欧斯塔基管功能障碍 (ETD) 延迟了AOM的分辨率,但SIRT3在这个过程中的作用尚不清楚.

研究的目的:

  • 研究SIRT3在LPS诱导的小鼠ETD中的作用.

主要方法:

  • 野生型 (WT) 和SIRT3淘汰 (SIRT3-KO) 鼠标的比较.
  • 尤斯塔基管 (ET) 结构的组织学分析.
  • 评估杯状细胞的增殖,MUC5AC分泌,乳毛长度,初始开口压力 (POP),粘膜细胞清除 (MCC) 和负压的活跃清除 (ACNP) 在LPS暴露后.

主要成果:

  • SIRT3-KO小鼠表现出加剧的LPS诱导的杯状细胞增殖和MUC5AC分泌.
  • 在SIRT3-KO小鼠中,毛长度减少,POP增加,MCC减少,ACNP受损.
  • 在LPS暴露后,SIRT3缺乏增加了对ET开放的抵抗力.

结论:

  • 在对LPS的反应中,SIRT3缺乏会使ETD恶化.
  • 升高的MUC5AC,增加的光液表面张力和受损的MCC功能,导致SIRT3-KO小鼠中ETD恶化.