硫福拉可以通过Nrf2/STAT3信号通路和肠道微生物群调节减轻DSS诱导的性结肠炎
Mengyuan Chen1, Gejun Yu1, Wentao Wu1
1School of Public Health, Health Science Center, Ningbo University, Ningbo, Zhejiang, 315211, P. R. China. hecanxia@nbu.edu.cn.
Food & function
|January 9, 2026
概括
硫福拉 (SFN) 通过调节Nrf2/STAT3通路和肠道微生物群来预防性结肠炎 (UC). Nrf2对于SFN至关重要.
科学领域:
- 胃肠病学 胃肠病学
- 分子生物学分子生物学
- 微生物学 微生物学
背景情况:
- 性结肠炎 (UC) 是一种慢性炎症性肠病.
- 甲 (SFN),来自十字花蔬菜,显示潜在的治疗益处.
- 核因子 (血红素衍生2) - - 类似2 (Nrf2) 和信号转换器和转录3 (STAT3) 途径的激活器都与UC病变有关.
研究的目的:
- 阐明SFN对硫酸 (DSS) 诱导的UC的保护作用背后的机制.
- 研究Nrf2和STAT3信号在SFN治疗作用中的作用.
- 探索SFN对UC肠道微生物群组成的影响.
主要方法:
- 对UC患者Nrf2和STAT3表达的GEO数据库的分析.
- 在体外研究中使用DSS诱导的Caco-2细胞模型与Nrf2siRNA.
- 使用DSS诱导的UC小鼠模型的体内研究,包括野生类型和Nrf2淘汰赛小鼠.
- 评估结肠病症状,炎症标志物,紧结蛋白和肠道微生物群组成.
主要成果:
- 患有UC的患者在结肠粘膜中表现出降低的Nrf2和升高的STAT3表达.
- 在Caco-2细胞和野生型小鼠中,SFN治疗缓解了UC症状,减少了炎症,并增强了紧结蛋白.
- 在Nrf2绝杀小鼠中,SFN的保护作用减弱.
- 在患有大肠炎的Nrf2淘汰小鼠中,SFN调节肠道微生物群组成,减少多样性和特定的细菌种群.
结论:
- SFN通过Nrf2/STAT3信号通路对DSS诱导的UC产生保护作用.
- Nrf2是SFN在UC治疗作用的关键调解者.
- SFN调节肠道微生物群,有助于其抗性结肠炎作用.
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