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在小鼠中,肠道微生物群通过HDAC2-ACSS2轴调节肝缺血-再输液损伤诱导的认知功能障碍
Yanbo Liu1, Zhen Li1, Tianning Sun1
1Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
CNS neuroscience & therapeutics
|February 9, 2024
概括
肝脏缺血-反损伤 (HIRI) 损害了海马中的乙酸代谢,导致认知功能障碍. 这种认知障碍和肠道失调可以通过便微生物移植传播.
科学领域:
- 神经科学是一个神经科学.
- 胃肠病学 胃肠病学
- 手术研究的研究.
背景情况:
- 肝脏缺血-再输损伤 (HIRI) 是肝脏手术中不可避免的并发症.
- 由HIRI引起的认知功能障碍与肠道微生物群失调有关.
研究的目的:
- 研究将HIRI,肠道失调和认知功能障碍联系在一起的机制.
- 探索HDAC2-ACSS2轴在与HIRI相关的认知障碍中的作用.
主要方法:
- 在C57BL/6小鼠中诱导肝缺血.
- 进行了肠道微生物移植.
- 与酶相关的免疫吸收试验和LC/MS被用于检测短链脂肪酸和乙-CoA.
主要成果:
- 在HIRI小鼠的海马中,ACSS2表达和酸盐代谢减少.
- 认知障碍和HDAC2-ACSS2轴失调是通过便微生物移植传播的.
- 在海马体中观察到降低的乙CoA和乙化素水平.
结论:
- 在HIRI之后,酸盐代谢在海马中受损,导致认知障碍.
- 肠道失调症通过影响基因素乙化,在HIRI诱导的认知功能障碍中起着至关重要的作用.
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