与牙周炎相关的代谢物伊索莱素损害了肠道屏障功能,并通过NF-κB信号传递加剧了肠道炎症反应
Xiaoxue Wang1, Yilin Luo1, Jie Ren1
1Department of Stomatology, The Eighth Affiliated Hospital, Southern Medical University (The First People's Hospital of Shunde, Foshan), Foshan, China.
Frontiers in cellular and infection microbiology
|December 15, 2025
概括
牙周炎相关的异质素 (Ile) 通过破坏肠道屏障和增加炎症而加剧结肠炎. 用IKK-16抑制NF-κB通路可以减轻这些有害影响,提供潜在的治疗见解.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 口腔医学是指口腔医学.
背景情况:
- 牙周炎与包括大肠炎在内的全身性疾病有关.
- 牙周炎中的代谢物异黄素 (Ile) 涉及到大肠炎的恶化.
- 确切的机制,由伊莱恶化大肠炎仍然不清楚.
研究的目的:
- 调查牙周炎相关的异黄素 (Ile) 如何加剧硫酸 (DSS) 诱导的大肠炎.
- 阐明NF-κB信号通路在Ile诱导的肠道炎症和屏障功能障碍中的作用.
- 评估抑制NF-κB激活的治疗潜力.
主要方法:
- 在C57BL/6J小鼠中建立实验性牙周炎和结肠炎模型.
- 评估结肠组织学,肠道透性 (FITC-dextran) 和紧结蛋白表达 (ZO-1,occludin).
- 通过qRT-PCR和西斑进行NF-κB信号通路激活的分析;IKK-16治疗效果的评估.
主要成果:
- 在结肠炎模型中,牙周炎和牙显著增加了肠道透性,并降低了紧结蛋白 (ZO-1,occludin) 的调节.
- 暴露于会增强肠道上皮细胞和有机体中的NF-κB信号传递.
- 在体外和体内,IKK-16治疗逆转了Ile诱导的肠道屏障损伤和炎症.
结论:
- 牙周炎通过损害肠道屏障功能并通过通过异黄素介导的NF-κB通路促进炎症来加剧结肠炎.
- 异黄素对肠道的有害影响与NF-κB信号的增强有关.
- 抑制NF-κB通路为牙周炎相关性结肠炎提供了潜在的治疗策略.
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