PI3K/Akt-Nrf2信号通路和粒细胞协同调解氧醇,以缓解肠道氧化损伤
Xiaobin Wen1, Shanlong Tang1, Fan Wan1
1State Key Laboratory of Animal Nutrition and Feeding, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
International journal of biological sciences
|September 9, 2024
概括
氧醇 (HT) 通过激活Nrf2通路并促进线粒消化,保护肠道免受氧化应激. 这些机制共同减少活性氧物种 (ROS),对HTT至关重要.
科学领域:
- 胃肠病学 胃肠病学
- 细胞生物学 细胞生物学
- 营养科学 营养科学
背景情况:
- 氧化应激是IBD和CRC等肠道疾病的关键因素.
- Nrf2通路和线粒减少活性氧物种 (ROS),但它们的相互作用尚未完全理解.
- 来自橄油的氧醇 (HT) 具有抗氧化特性,具有潜在的治疗应用.
研究的目的:
- 在猪模型中研究HT对肠道氧化损伤的影响.
- 阐明HT的保护作用的潜在机制,重点关注Nrf2通路和线粒.
- 在HT的抗氧化作用中探索Nrf2和线粒细胞衰变之间的协同关系.
主要方法:
- 在猪模型和IPEC-J2细胞中使用Diquat (DQ) 诱导氧化应激.
- 给出Hydroxytyrosol (HT) 来评估其对DQ诱导损伤的保护作用.
- 涉及PI3K/Akt-Nrf2信号通路和线粒评估的机制研究.
- 抑制研究以证实Nrf2和线粒细胞衰减在HT疗效中的作用.
主要成果:
- 治疗HT缓解了迪卡特诱导的氧化应激,改善了肠道屏障功能.
- HT激活了PI3K/Akt-Nrf2信号通路,并促进了肠道细胞中的线粒.
- 干扰Nrf2通路或线粒消化消除了HT的保护作用,表明了协同作用的关系.
- 通过Nrf2介导的抗氧化酶诱导和由髓细胞驱动的ROS降低对于HT的作用至关重要.
结论:
- 通过Nrf2通路和线粒细胞衰变的协同作用,HT对肠道氧化应激具有保护作用.
- 通过Nrf2和线性来维持肠道氧化还原平衡对于减轻氧化损伤至关重要.
- 针对Nrf2和线粒细胞衰变通路,可能与HT,为与氧化压力相关的肠道疾病提供了一个有前途的治疗策略.
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