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在实验性死性肠球炎中,NAMPT抑制通过调节巨细胞激活来缓解肠炎

Qianyang Liu¹, Kai Gao², Xionghui Ding³

¹Department of Pediatrics, Chongqing Health Center for Women and Children, Chongqing, China; Department of Pediatric Surgery, Chongqing Health Center for Women and Children, Chongqing Medical University, Chongqing 400054, China; Department of Obstetrics and Gynecology, Women and Chidren's Hospital, Chongqing Medical University, Chongqing, China.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

|June 17, 2023

概括

使用FK866抑制尼古丁胺胺酸转移酶 (NAMPT) 通过调节巨分极和NAD+水平,降低了肠道炎症,并改善了死性肠球炎 (NEC) 模型的结果.

科学领域:

胃肠病学胃肠病学
免疫学免疫学免疫学
新生儿研究新生儿研究

背景情况:

结核性肠球炎 (NEC) 是早产婴儿的一种严重的肠道疾病.
尼古丁胺酸转移酶 (NAMPT) 在与NEC相关的肠炎症中的作用尚未完全理解.
消耗NAD+的酶与免疫反应有关.

研究的目的:

研究NAMPT抑制对实验性死性肠球炎 (NEC) 中肠粘膜免疫的作用.
为了确定FK866,一个特定的NAMPT抑制剂,可以减轻NEC病原体.
探索NAMPT抑制对巨细胞两极化和NEC中NAD+代谢的影响.

主要方法:

在人类NEC阴茎样本中评估NAMPT表达.
给试验NEC幼使用FK866.
测量细胞间NAD+水平和NAD+依赖酶的表达 (PARP1,Sirt6).
评估了巨细胞极化 (M1) 和细胞/抗菌活性.
使用NMN补充剂恢复NAD+水平.

主要成果:

在人类NEC骨髓中,NAMPT表达升高.
在幼中,FK866治疗减弱了M1巨细胞两极分化,并减少了NEC症状.
FK866抑制了细胞间的NAD+水平和PARP1和Sirt6.6的表达.
巨细胞和抗菌活性受到FK866的损害,但被NMN恢复.
FK866减少了肠道巨细胞的透,并改变了巨细胞的两极分化.

结论:

由FK866抑制NAMPT通过减少肠道炎症改善实验NEC.
FK866调节巨细胞两极分化和NAD+代谢,影响NEC的先天免疫力.
向NAMPT可能是死角性肠球炎的治疗策略.

关键词:

在FK86666中使用.巨细胞是一个巨细胞.它们是NAD+NAD+NAD.这个名字叫做NAMPT.NEC NEC NEC是指一个国家.

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