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E. Coli Nissle 1917 减轻抗生素中介的神经毒性 可能通过斑马鱼的肠-大脑轴
Vajagathali Mohammed1, Meenakshi Shanmugaraja2
1Faculty of Allied Health Sciences, Chettinad Academy of Research and Education, Chettinad Hospital and Research Institute, Kelambakkam, 603103, India.
Applied biochemistry and biotechnology
|March 2, 2026
概括
常见的抗生素会伤害肠道细菌和大脑健康. 益生菌大肠杆菌尼斯尔1917 (EcN1917) 通过保护肠道微生物群和支持肠-大脑轴,保护斑马鱼免受抗生素诱导的神经毒性.
科学领域:
- 微生物学 微生物学
- 神经科学是一个神经科学.
- 药理学 药理学 是一个学科.
背景情况:
- 过度使用抗生素会破坏肠道微生物群,影响肠-大脑轴.
- 神经健康越来越多地与肠道微生物群有关.
- 益生菌的神经保护作用需要进一步研究.
研究的目的:
- 研究常见抗生素的神经行为和生物化学效应.
- 评估益生菌大肠杆菌尼斯尔1917 (EcN1917) 对抗生素诱导的神经毒性的神经保护潜力.
- 阐明肠-大脑轴在调解这些影响中的作用.
主要方法:
- 对斑马鱼进行了抗菌,神经行为和生化分析,这些斑马鱼暴露在阿莫西西林,阿齐思罗米辛,西普罗夫洛克萨,里芬素和氧化四环素中.
- 通过向暴露于抗生素的斑马鱼施用 EcN1917 来评估神经保护.
- 使用Lactobacillus rhamnosus (L. rhamnosus) 的体外研究检查了EcN1917对抗生素挑战期间随期生存的影响.
主要成果:
- 抗生素显著影响了斑马鱼的行为,并导致大脑组织损伤,包括氧化应激和炎症.
- 在斑马鱼中,EcN1917的使用改善了行为缺陷,并减轻了脑组织损伤.
- 在抗生素挑战期间,EcN1917促进了L. rhamnosus的生存,这表明了一种涉及肠道微生物群保存的机制.
结论:
- 大肠杆菌尼斯尔1917 (EcN1917) 在减轻抗生素诱导的神经毒性方面显示出显著的治疗潜力.
- 通过维护肠道微生物群,EcN1917的神经保护作用可能通过肠-大脑轴进行介导.
- EcN1917可以提供一种策略来抵消与抗生素使用相关的神经副作用.
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