由于急性损伤而破坏转硫路径会导致肠道损伤
Shunshun Jin1,2, Charith U B Wijerathne1,2, Yaw L Siow3,4
1Laboratory of Integrative Biology, St. Boniface Hospital Research Centre, Winnipeg, MB R2H 2A6, Canada.
iScience
|October 2, 2025
概括
急性损伤 (AKI) 扰乱了转硫路径,减少了肠道中的关键抗氧化剂,如谷氨. 这导致肠道屏障功能受损和AKI的肠道失调.
科学领域:
- 胃肠病学 胃肠病学
- 腎臟病學 (nephrology) 是一種醫學專業.
- 生物化学 生物化学
背景情况:
- 急性损伤 (AKI) 与肠道功能障碍有关.
- 氧化应激在AKI引起的肠损伤中起着关键作用.
- 转硫化途径对于通过谷氨合成的抗氧化防御至关重要.
研究的目的:
- 调查AKI导致肠道损伤的机制.
- 探索转硫途径在与AKI相关的肠损伤中的作用.
主要方法:
- 在Sprague-Dawley大鼠中,通过缺血-再输液诱导了AKI.
- 评估了肠道谷氨水平,屏障功能和酶表达.
- 分析了肠道微生物群组成和细菌酶表达.
主要成果:
- AKI显著降低了肠道中的谷氨水平,并损害了屏障完整性.
- 关键的转硫酶 (CBS,CSE) 的表达在肠表皮减少.
- AKI改变了肠道微生物群和细菌酶表达,影响了抗氧化剂防御.
结论:
- 转硫化通路的破坏有助于在AKI中损害肠道屏障.
- 缺陷的谷氨生物合成和改变的肠道微生物群是关键机制.
- 向转硫化通路可能为AKI诱导的肠损伤提供治疗策略.
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