在DSS诱导的结肠炎中Aucubin的保护作用:调节炎症通路,肠道屏障完整性和肠道微生物群
Yong Zhang1, Han Qiao1, Yuxin Cao1
1Institute for Biological Engineering, Henan University of Technology, Zhengzhou 450001, China.
Foods (Basel, Switzerland)
|November 13, 2025
概括
阿库 (AU) 通过改善肠道屏障功能和减少炎症,有效地缓解小鼠的结肠炎. 这种天然化合物也积极调节肠道微生物群,为炎症性肠道疾病的治疗提供了潜力.
科学领域:
- 药理学和胃肠病学 药理学和胃肠病学
- 自然产品研究自然产品研究
- 微生物组研究 微生物组研究
背景情况:
- 奥库 (Aucubin,AU) 是从Eucommia叶中提取的,它具有已知的抗炎和抗氧化特性.
- 有限的研究存在于AU在治疗大肠炎,一个重要的炎症性肠病的疗效.
- 了解AU对结肠炎的治疗潜力对于开发新型治疗非常重要.
研究的目的:
- 在小鼠模型中研究aucubin (AU) 对硫酸 (DSS) 诱导的大肠炎的治疗作用.
- 评估AU对肠道屏障完整性,炎症标志物和肠道微生物群组成的影响.
- 探索AU在缓解大肠炎中的潜在分子机制.
主要方法:
- 在使用DSS给药的小鼠中建立了结肠炎模型.
- 用于评估其对疾病活动指数 (DAI),器官指数和结肠形态学的影响.
- 通过RT-qPCR分析了抗氧化酶 (SOD,GSH-PX,CAT),脂质过氧化 (MDA),炎症细胞因子 (IL-1β,TNF-α,IL-18) 和肠道屏障基因 (OCLN,CLDN1,CLDN2,ZO-2,MUC1) 的血清和结肠水平.
- 使用16S rRNA测序研究了AU对肠道微生物群组成的影响.
- 进行了体外细胞实验,以评估AU对肠道屏障基因 (MUC2,ZO-1,OCLN,CLDN1),炎症细胞因子 (IL-1β,TNF-α),抗炎因素 (IL-10) 和关键信号通路分子 (IL-1R,MyD88,TAK1,IKKα,RelA) 的影响.
主要成果:
- AU治疗显著降低了DAI得分和器官指数,恢复了结肠形态,并增加了抗氧化酶水平 (SOD,GSH-PX,CAT),同时降低了DSS诱导的大肠炎小鼠的MDA水平.
- AU降低了促炎因素 (IL-1β,TNF-α,IL-18,MyD88,NF-κB) 的表达,并上调了与肠道屏障相关的基因 (OCLN,CLDN1,CLDN2,ZO-2,MUC1).
- AU调节了肠道微生物群,增加了有益的细菌 (Bacteroidota, Firmicutes, Verrucomicrobiota) 并减少了有害的细菌 (Proteobacteria, Deferribacterota).
- 在体外研究证实了AU增强肠道屏障基因表达的能力,减少促炎细胞因子,增加IL-10,并抑制关键炎症信号通路 (NF-κB通路).
结论:
- 奥库 (Aucubin,AU) 通过加强肠道屏障,减少炎症和重新平衡肠道微生物群,在缓解DSS诱导的大肠炎方面显示出显著的治疗潜力.
- AU至少部分通过调节NF-κB信号通路来发挥其保护作用.
- 这些发现为AU作为炎症性肠病治疗的发展提供了坚实的理论和技术基础.
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