益生菌通过调节产生丁酸盐的肠道细菌来减轻帕金森病中类似抑郁的行为,神经炎症和突触可塑性
Ingrid Prata de Mendonça1,2, Rodrigo Soares da Silva1,2, Igor Henrique Rodrigues de Paiva1,2
1Laboratory of Ultrastructure, Aggeu Magalhães Institute (IAM), Recife, PE, Brazil.
Inflammopharmacology
|March 13, 2026
概括
果醇糖 (FOS) 和银醇糖 (GOS) 益生菌通过增加有益的肠道细菌和丁酸盐水平来缓解帕金森病的运动和抑郁症状. 这种方法还可以减少神经炎症,并改善大脑中的突触可塑性.
科学领域:
- 神经科学是一个神经科学.
- 胃肠病学 胃肠病学
- 药理学 药理学是指药理学的学科.
背景情况:
- 帕金森病 (PD) 呈现出运动和非运动症状,如抑郁症,影响生活质量.
- 微生物群-肠-大脑轴越来越多地与PD和抑郁症有关.
- 益生菌纤维,如果寡糖 (FOS) 和银寡糖 (GOS),调节肠道微生物群,并产生短链脂肪酸 (SCFA).
研究的目的:
- 为了研究FOS和GOS在罗丁诱导的帕金森病模型上的治疗效果.
- 评估FOS和GOS对运动功能的影响,类似抑郁症的行为,以及肠-大脑轴标记.
主要方法:
- 将FOS和GOS给罗诺诱导的PD大鼠模型.
- 分析运动和类似抑郁的行为.
- 测量神经递质水平 (血清素),肠道微生物群组成,SCFA (酸盐) 水平,肠道完整性标记物,神经炎症标记物和脑组织和血清中的神经可塑性指标.
主要成果:
- 在PD模型大鼠中,FOS和GOS治疗显著改善了运动症状,并减少了类似抑郁症的行为.
- 益生菌的使用增加了产生SCFA的肠道细菌,从而导致血清和大脑中酸盐水平的提高.
- FOS和GOS减弱了α-synuclein积累,降低了神经炎症 (降低了IBA-1,GFAP,iNOS,p-NFkB,IL1-β),并改善了肠道屏障功能 (增加了zonula occludens,occludin).
- 通过上调酸盐受体 (GPR43,GPR109),BDNF,p-CREB和PSD-95的调节,治疗增强了神经可塑性,同时保留了黑色物质中的多巴胺基神经元.
结论:
- 在PD模型中,FOS和GOS有效地改善了类似抑郁症的行为和运动缺陷.
- 这些益生菌调节肠道微生物群,增加有益的SCFA,特别是酸盐.
- FOS和GOS通过减少神经炎症,改善肠道屏障完整性和增强帕金森病的神经可塑性来产生神经保护作用.
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