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谷氨素-1调节NF-κB信号通路,以激活可诱导的氧化合成酶在实验性死性肠球炎中

Yunfei Zhang^1,2, Mei Yan¹, Yingying Xia^3,4

¹Pediatric Center of the First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, P.R. China.

Molecular therapy. Methods & clinical development

|March 18, 2024

概括

葡萄糖素-1 (Grx1) 缺乏通过抑制NF-κB通路来保护人免受死性肠球炎 (NEC) 的侵害. 移除Grx1可以减少炎症和肠道损伤,这表明Grx1是NEC的治疗点.

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:

结核性肠球炎 (NEC) 涉及肠道炎症和屏障损伤,诱导性氧化合成酶 (iNOS) 和核因子kappa B (NF-κB) 起着关键作用.
NF-κB通路由抑制性kB激酶β (IKKβ) 调节,并且可以通过S-氨基化调节,这是一个由谷氨素-1 (Grx1) 影响的过程.

研究的目的:

调查Grx1在实验性死性肠球炎 (NEC) 中的作用.
在NEC模型中确定 Grx1 除是否影响 iNOS,NF-κB 信号和肠道损伤.

主要方法:

使用了野生类型和Grx1-淘汰赛小鼠,接受了NEC诱导疗法.
用脂多糖 (LPS) 处理的初级肠上皮细胞 (IECs).
评估了iNOS,氧化 (NO),活性氧物种 (O2·-),NF-κB激活,炎症,亡以及肠道屏障完整性.

主要成果:

与野生类型小鼠相比,Grx1淘汰赛 (Grx1-/-) 小鼠表现出减弱的NEC严重性.
Grx1 除增强了 IKKβ 谷氨基化,导致 NF-κB 失活.
在Grx1-/-小鼠中观察到iNOS,NO和O2·-的产生减少,以及促炎性细胞因子的减少,细胞亡,以及改善肠道屏障功能和增殖.

结论:

通过IKKβ的S-氨基基化抑制iNOS和NO通路,从而抑制NF-κB信号传递,Grx1剥离可以防止NEC.
Grx1及其相关的信号通路代表了管理死性肠球炎的潜在治疗标.

关键词:

这就是NF-κBB.在S-Glutathionylation的过程中,葡萄糖素-1-1的使用.可以诱导的氧化合成酶.死性肠球炎 (necrotizing enterocolitis) 是一种致死性肠球炎的疾病.氧化应激是一种氧化应激.

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