在性结肠炎模型小鼠中,naringin通过调节JAK2/STAT3信号通路来改善肠道损伤
Miaomiao Wu1, Yating An2, Yongmin Li3
1College of Pharmacy, Hebei North University, Zhangjiakou, Hebei 075000, P.R. China.
Molecular medicine reports
|January 23, 2026
概括
纳林素是一种天然的黄类化合物,通过恢复肠道屏障功能和减少炎症,有效治疗性结肠炎 (UC). 它通过抑制Janus激酶2 (JAK2) /信号转换器和转录3 (STAT3) 途径的激活器来起作用,为UC提供了一个有前途的新疗法.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- 性结肠炎 (UC) 是一种慢性自身免疫性疾病,导致肠道炎症和屏障功能障碍.
- 目前的UC治疗有局限性和不良影响,需要新的治疗策略.
- 纳林因是一种类黄素,具有抗炎性质,但其在UC中的机制,特别是通过JAK2/STAT3通路,尚不清楚.
研究的目的:
- 在小鼠模型中研究纳林丁对硫酸 (DSS) 诱导的性结肠炎 (UC) 的治疗作用.
- 阐明纳林因在调节UC中Janus激酶2 (JAK2) /信号转换器和转录3 (STAT3) 激活器信号通路中的作用.
- 评估naringin对UC肠道屏障完整性和功能的影响.
主要方法:
- 使用了DSS诱导的大肠炎小鼠模型和IL-6刺激的Caco-2细胞系.
- 小鼠接受了纳林金或梅萨拉的DSS;疾病活性指数 (DAI),组织病理学,紧结蛋白 (ZO-1,奥克卢丁) 和JAK2 / STAT3激活被评估.
- 使用体电阻 (TEER) 和FD-4透性试验评估Caco-2细胞屏障功能,使用STAT3沉默证实通路参与.
主要成果:
- 纳林因显著降低了体重减轻,结肠缩短,DAI和DSS诱导的大肠炎中的组织学损伤.
- 纳林林治疗恢复了紧结蛋白ZO-1和奥克卢丁的表达,并抑制了结肠组织中的JAK2/STAT3酸化.
- 在Caco-2细胞中,naringin逆转了IL-6诱导的屏障功能障碍,并增强了紧密结合的完整性,而STAT3沉默进一步支持通路参与.
结论:
- 纳林因通过减轻炎症和恢复肠道屏障功能,对性结肠炎 (UC) 具有显著的治疗潜力.
- 该机制涉及抑制JAK2 / STAT3通路激活,从而改善肠道屏障完整性.
- 纳林代表了UC的有前途的新型治疗剂,需要进一步的临床研究.
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