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受损的NHE8表达是维生素D缺乏引起的肠壁功能障碍的原因

Yaoyu Guo¹, Yanni Li¹, Zeya Tang²

¹Department of Gastroenterology and Hepatology, West China Hospital, Sichuan University, Chengdu 610041, China.

|November 25, 2023

概括

维生素D (VitD) 和它的受体 (VDR) 通过上调NHE8表达来保护肠道,这对于预防性结肠炎 (UC) 恶化至关重要. 损坏的NHE8功能加剧了UC,突出了其治疗潜力.

科学领域:

胃肠病学胃肠病学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

性结肠炎 (UC) 涉及肠道屏障功能障碍.
维生素D (VitD) 和它的受体 (VDR) 与肠道健康有关.
Na+/H+交换器异型8 (NHE8) 对于肠道平衡至关重要,也是潜在的UC治疗标.

研究的目的:

研究VitD/VDR在调节NHE8表达以保护肠道中的作用.
阐明在UC中VitD/VDR介导的肠道保护背后的分子机制.

主要方法:

使用VitD缺乏,VDR淘汰 (VDR-/-) 和NHE8淘汰 (NHE8-/-) 的DSS诱导大肠炎的小鼠模型.
在体外机理学研究中使用了Caco-2细胞和3D体.
研究了VDR调制 (siRNA,过度表达) 和TNF-α/NF-κb信号抑制 (QNZ) 对NHE8表达的影响.

主要成果:

帕里卡尔西托尔 (一种VitD类似物) 在大肠炎小鼠中调节了NHE8并恢复了结肠粘膜.
维生素D缺乏或VDR淘汰会影响NHE8表达和恶化的结肠炎.
缺乏NHE8使得小鼠对帕里卡尔西托尔的保护作用没有反应.
VDR敲击加剧了TNF-α诱导的NHE8下调和NF-κb激活,这是QNZ阻止的.

结论:

抑郁的NHE8表达有助于加剧VitD缺乏引起的结肠炎.
VitD/VDR信号通过NHE8.8的调节,至少部分地保护肠道屏障.
NHE8代表了UC治疗策略的新型分子标.

关键词:

Na+/H+交换器异型8的同型肠道屏障的功能肠道屏障的功能性结肠炎是一种维生素D是维生素D的重要组成部分.维生素D受体是维生素D的受体.

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