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原蛋白通过对Nrf2-介导的紧结完整性进行升级来缓解肠道缺血/再输液损伤
Bin Xu1,2,3, Yan Zhuang2, Ying Zhang4
1Department of Physiology, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Molecular nutrition & food research
|March 28, 2025
概括
作为一种天然化合物,apigenin通过减少氧化应激和炎症来保护肠道免受损伤. 它通过激活Nrf2增强了肠道屏障功能,为缺血/再输伤提供了潜在的治疗方法.
科学领域:
- 胃肠病学 胃肠病学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 肠道缺血/反 (I/R) 损伤涉及上皮质屏障功能障碍.
- Nrf2介导的氧化应激是I/R损伤的关键调节者.
- 在肠道I/R损伤中,阿皮基宁的作用尚不清楚.
研究的目的:
- 为了研究阿皮基宁对肠道I/R损伤的影响.
- 通过激活Nrf2信号来确定阿皮基宁是否可以改善肠道屏障功能障碍.
主要方法:
- 在体内 (老鼠模型) 和体内 (Caco-2和IEC-6细胞) 建立了肠道I / R的模型.
- 给药的阿皮基宁和评估的炎症性细胞因子,氧化应激标志物和屏障功能.
- 分析了Nrf2,HO-1和紧结蛋白的表达.
主要成果:
- 在I/R损伤中,阿皮原蛋白显著地保护了肠道粘膜损伤.
- 原蛋白抑制了炎症性细胞因子和氧化应激标志物.
- 通过对Nrf2,HO-1和紧结蛋白进行上调,阿皮基宁改善了屏障功能障碍.
- Nrf2的敲击取消了apigenin的保护作用.
结论:
- 原素预处理缓解了肠道I/R诱导的屏障损伤.
- 保护机制涉及Nrf2激活和紧接口上调.
- 在I/R相关的肠道疾病中,apigenin具有潜在的治疗策略.
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