I3C通过激活AhR-Nrf2-SLC7A11-GPX4通路来抑制铁亡,从而保护IPEC-J2细胞
Haoran Jiang1, Yalei Zhang1, Xiwen Hu1
1College of Tropical Agriculture and Forestry, Hainan University, Danzhou 571737, China.
International immunopharmacology
|December 12, 2025
概括
印醇-3-碳醇 (I3C) 通过激活烯碳化合物受体 (AhR) 和Nrf2通路来保护小猪肠道屏障功能,抑制铁和减少炎症.
科学领域:
- 胃肠病学 胃肠病学
- 细胞生物学 细胞生物学
- 分子机制的分子机制
背景情况:
- 断奶压力会损害小猪的肠上皮质屏障功能.
- 印醇-3-碳醇 (I3C) 显示出通过烯碳化合物受体 (AhR) 激活减轻肠道屏障损伤的潜力,但机制尚不清楚.
研究的目的:
- 研究I3C激活的AhR如何调节Nrf2-SLC7A11-GPX4通路.
- 阐明I3C在缓解IPEC-J2细胞中的屏障功能障碍和铁亡中的作用.
主要方法:
- 转录组测序和KEGG分析以确定受影响的途径.
- 抑制铁,AhR和Nrf2通路,以评估I3C的影响.
- 评估炎症反应,抗氧化能力,紧密结形成和铁灭症标志物.
主要成果:
- I3C减轻了LPS诱导的损伤,并提高了AhR和铁亡途径的调节.
- 抑制铁亡减少了炎症,增强了抗氧化能力,并增加了紧密的结节.
- 阻断AhR和Nrf2逆转了I3C的保护作用,增加了屏障功能障碍和铁亡.
结论:
- 在IPEC-J2细胞中,I3C减轻了LPS诱导的肠壁损伤.
- 保护机制涉及Nrf2-SLC7A11-GPX4通路的AhR介导激活.
- I3C抑制铁,从而减轻肠道屏障功能障碍.
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