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HDAC3通过调节肠道质细胞的cGAS-Sting通路来改善小鼠的肠道功能

Pu Li¹, Zhaohui Zheng², Jing Qi³

¹Department of Critical Care Medicine, The Second Affiliated Hospital of Air Force Medical University, Xi'an 710038, Shaanxi, China.

Molecular immunology

|September 4, 2023

概括

基脱乙酶3 (HDAC3) 抑制通过调节肠质细胞中的cGAS-Sting通路,减少炎症和亡,改善严重的急性胰腺炎 (SAP).

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:

严重的急性胰腺炎 (SAP) 是一种严重的疾病,具有显著的肠道损伤.
海斯脱乙酶3 (HDAC3) 在SAP病变发生中的作用目前尚不清楚.
HDAC3与各种细胞过程和疾病有关.

研究的目的:

研究HDAC3在SAP中的作用和机制.
探索HDAC3作为SAP的潜在治疗点.

主要方法:

建立了一个严重的急性胰腺炎 (SAP) 鼠标模型.
利用免疫组织化学,H&E染色,RT-qPCR和西部斑点来评估HDAC3表达和肠道病理.
采用了细胞亡套件和ELISA来测量细胞亡率和炎症因素.
研究了cGAS-Sting通路激活和肠道屏障功能.

主要成果:

在SAP患者和小鼠中,HDAC3,cGAS和Sting表达升高.
沉默HDAC3减少了肠道上皮细胞的亡和炎症,抑制了氧化应激,并促进了质细胞的增殖和粘附.
沉默HDAC3抑制了肠道质细胞中的cGAS-Sting通路激活.
在SAP小鼠中,抑制HDAC3改善了肠道屏障功能.

结论:

在SAP病变发生过程中,HDAC3起着至关重要的作用.
针对HDAC3,特别是通过肠道质细胞中的cGAS-Sting通路,为SAP提供了一个有前途的治疗策略.
抑制HDAC3可以缓解肠道损伤,并改善实验SAP的结果.

关键词:

在CGAS-sting上进行了调查.在 HDAC3 中,HDAC3 是氧化应激是一种氧化应激.严重的急性胰腺炎

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