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维护肠道上皮细胞,以激活M2巨细胞,以抵抗脱氧尼瓦伦醇损伤

Shijie Fan¹, Jiaying Chen¹, Huihui Tian¹

¹State Key Laboratory of Animal Nutrition and Feeding, Institute of Animal Sciences of Chinese Academy of Agricultural Sciences, Beijing, 100193, China.

Free radical biology & medicine

|April 18, 2024

概括

(Se) 通过抑制铁和激活M2巨细胞来保护肠道免受脱氧 (DON) 损伤. 这改善了肠道屏障功能,增强了抗炎能力,这对肠道平衡至关重要.

科学领域:

胃肠病学胃肠病学
免疫学免疫学免疫学
毒理学毒理学毒理学

背景情况:

脱氧尼瓦伦醇 (DON) 诱导的肠道损伤对健康构成重大风险.
(Se) 以其对各种伤害的保护作用而闻名.
表皮细胞-M2巨细胞通路在DON引起的损伤中的作用需要进一步阐明.

研究的目的:

为了研究 (Se) 对脱氧尼瓦伦醇 (DON) 诱导的肠损伤的保护作用.
探索通过Se.调节上皮细胞-M2巨细胞通路的调节.
确定参与DON诱导的肠道炎症的关键分子通路.

主要方法:

在体内研究中,小鼠模型接受了DON和Se补充剂.
使用MODE-K细胞进行体外研究.
对关键蛋白质 (GPX4,p-PI3K,AKT),铁亡标记物 (4-HNE),炎症性细胞因子 (IL-6) 和巨标记物 (CSF-1,M2巨) 的分析.
使用铁灭抑制剂 (Fer-1) 来验证途径的参与.

主要成果:

补充Se改善了肠道屏障功能,并降低了血清DON水平.
Se增加了GPX4,p-PI3K和AKT,同时抑制了铁 (4-HNE).
在DON引起的肠炎症中,GPX4-PI3K/AKT-ferroptosis通路至关重要.
Se激活了CSF-1-M2巨轴,降低了IL-6并增强了抗炎能力.

结论:

(Se) 通过GPX4-PI3K/AKT-ferroptosis路径减轻脱氧 (DON) 诱导的肠损伤.
通过通过CSF-1轴促进M2抗炎巨细胞来增强肠道平衡.
这项研究强调了一种新的肠上皮细胞调节M2巨细胞的机制.

关键词:

在CSF-1M2巨细胞轴上.脱氧尼瓦伦醇 (deoxynivalenol) 是一种除氧化物.铁性化 (ferroptosis) 是一种在GPX4中使用GPX4.肠道上皮细胞肠道上皮细胞是一种.

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