黑色素B通过脏-肠道微生物群-大脑轴在APP/PS1模型小鼠中缓解认知障碍
Jiahui Jiang1, Jiahang Deng1, Yuntao Zhao1
1College of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Province Engineering Laboratory for Marine Biological Products, Zhanjiang Municipal Key laboratory of Marine Drugs and Nutrition for Brain Health, Zhanjiang 524088, China.
International immunopharmacology
|April 7, 2025
概括
黑色素B (HB) 通过调节迷走神经--肠轴来改善阿尔茨海默病 (AD) 的症状. 这种天然化合物调节肠道微生物群并减少神经炎症,为AD提供治疗潜力.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 阿尔茨海默病 (AD) 病原发生涉及大脑-脏和肠道微生物群-大脑轴.
- 甲基乙烯 (HB) 曾经显示出在修复脏Th1/Th2不平衡和改善AD小鼠的认知缺陷方面的潜力.
- 在阿尔茨海默氏症中,HB对迷走神经-脏电路的影响仍未得到研究.
研究的目的:
- 通过-肠微生物群-大脑轴研究HB在阿尔茨海默病 (AD) 中的治疗机制.
- 为了确定HB的效应是否依赖于迷走神经-脏电路.
- 探索HB在神经退行性疾病中调节神经免疫肠道电路的潜力.
主要方法:
- 利用APP/PS1小鼠,有或没有骨缩 (SD) 来评估HB的机制.
- 使用新型对象识别 (ORT) 和对象位置记忆 (OLT) 测试评估认知功能.
- 分析了Aβ斑块,化陶 (p-Tau),神经炎症,脏淋巴细胞,肠道屏障完整性和肠道微生物群组成 (16S rRNA测序).
主要成果:
- 服用HB显著改善了认知表现,并降低了大脑和血清中的Aβ1-42和p-Tau水平.
- 乙型肝炎降低了脏Th1/Th2比率,缓解了肠道透性,并减少了神经炎症.
- 这些HB的有益作用被废除在骨缩 (SD) 的小鼠,肠道微生物群的分析显示HB诱导的有益细菌的丰富和病原性物种的抑制.
结论:
- 这项研究提供了第一个证据,证明HB通过对-肠微生物群-大脑轴的迷走神经依赖调节来改善AD病理.
- 在神经退行性疾病中,HB证明了神经-免疫-肠道电路调节的多模式治疗潜力.
- 这些发现突显了HB作为向阿尔茨海默病相互连接的途径的有希望的代理人.
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