一个肠道微生物群 - 胆酸轴在阿司匹林介导的损伤后促进肠道平衡
Ting Li1, Ning Ding1, Hanqing Guo2
1Department of Cardiovascular Medicine, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, China; Key Laboratory of Molecular Cardiology, Xi'an, Shaanxi, China; Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi'an, Shaanxi, China.
阿司匹林抑制有益的肠道细菌,如Parabacteroides goldsteinii,导致肠道受损. 补充P.goldsteinii或其代谢物7-keto-lithocholic acid通过对抗FXR受体来保护肠道屏障.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 代谢学 代谢学 代谢学
背景情况:
- 阿司匹林使用与胃肠道损伤有关.
- 阿司匹林改变肠道微生物群和胆酸 (BA) 代谢,影响肠道平衡.
- 具体的机制尚不清楚.
研究的目的:
- 研究阿司匹林对肠道微生物群和胆汁酸的影响.
- 为了确定能够减轻阿司匹林诱导的胃肠道损伤的微生物代谢物.
- 阐明这些代谢物在肠道修复中的作用.
主要方法:
- 对临床队列和阿司匹林治疗小鼠模型的分析.
- 受阿司匹林影响的肠道微生物的识别和表征.
- 用Parabacteroides goldsteinii及其代谢物7-keto-lithocholic acid (7-keto-LCA) 进行补充研究.
- 调查7-基托-LCA对肠上皮质修复和信号通路 (FXR,Wnt) 的影响.
主要成果:
- 阿司匹林抑制了Parabacteroides金石菌的生长.
- 用P. goldsteinii或7-keto-LCA补充剂减少了阿司匹林诱导的肠损伤和肠道屏障功能障碍.
- 这些保护作用取决于7-基托-LCA的产生.
- 7-基托-LCA 作为FXR 抗剂,促进 Wnt 信号传递和肠干细胞自我更新.
结论:
- 阿司匹林会破坏肠道微生物群,特别是抑制P. goldsteinii.
- 黄金菌的代谢物7-基托-LCA可以防止阿司匹林诱导的肠道损伤.
- 7--LCA通过对抗FXR和增强Wnt信号来促进肠道修复,突出了在阿司匹林治疗期间维持肠道平衡的新机制.
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