印度尔-3-酸对睡眠剥夺引起的认知障碍产生保护作用
Jiao Han1, Linjuan Zhang2, Yixuan Lyu1
1Department of Anesthesiology and Perioperative Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China; Center for Brain Science, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.
Neuropharmacology
|October 31, 2025
概括
睡眠不足会通过减少肠道代谢物英多尔-3-酸 (IAA) 来影响认知. 补充IAA通过增强肠-大脑轴信号通路来恢复认知功能.
科学领域:
- 神经科学是一个神经科学.
- 微生物学 微生物学
- 代谢学 代谢学 代谢学
背景情况:
- 睡眠不足 (SD) 与认知缺陷和降低海马神经发生有关.
- 人们已经认识到肠道微生物群在SD引起的认知障碍中的作用,但信号通路尚不清楚.
研究的目的:
- 研究肠道微生物代谢物在睡眠剥夺引起的认知缺陷中的作用.
- 阐明连接肠道代谢物与海马功能的信号机制.
主要方法:
- 在被睡眠剥夺的雄性小鼠中进行了多个omics分析.
- 通过口服的英多尔-3-酸 (IAA) 评估其对认知功能和肠道完整性的影响.
- 研究涉及酸受体 (AhR) 和血清素 (5-HT) 信号传递的机制性途径.
主要成果:
- 睡眠不足显著降低了小鼠的英多尔-3-酸 (IAA) 水平.
- 口服IAA给药改善了SD小鼠的认知障碍,并恢复了肠道完整性.
- IAA通过AhR和血清素 (5-HT) 释放激活肠-EC-静脉神经-大脑轴,促进海马神经发生.
结论:
- 来自肠道的英多尔-3-酸 (IAA) 在调节海马功能和认知表现方面发挥着关键作用.
- 肠-EC-阴道神经-大脑轴是IAA影响神经行为结果的关键通路.
- 针对IAA介导的肠-大脑轴为睡眠剥夺引起的认知障碍提供了潜在的治疗策略.
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