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干的TNF-α调节:对肠道微生物群稳定性和衰老中的认知健康的影响

Jianfei Mu¹, Qinlu Lin², Shuang Wang¹

¹Molecular Nutrition Branch, National Engineering Research Center of Rice and By-product Deep Processing, College of Food Science and Engineering, Central South University of Forestry and Technology, Changsha, Hunan, P.R. China.

NPJ biofilms and microbiomes

|October 9, 2025

概括

粉KF-8通过调节肠道微生物群和减少神经炎症,改善老年小鼠的认知功能. 它稳定了Akkermansia muciniphila (AKK) 并抑制TNF-α,促进健康的衰老.

科学领域:

神经科学是一个神经科学.
微生物学微生物学
老年学是一门学科.

背景情况:

与衰老相关的神经炎症有助于认知能力下降.
肠道微生物群和生物活性化合物在这一过程中的作用尚未完全理解.
粉KF-8是一种潜在的肠道微生物群调节剂.

研究的目的:

为了研究粉KF-8减轻与年龄相关的神经炎症和认知衰退的机制.
确定肠道微生物群,特别是Akkermansia muciniphila (AKK) 在KF-8的影响中的作用.
阐明TNF-α在KF-8介导的神经保护中的参与.

主要方法:

给老年小鼠使用大米皮质KF-8.
抗生素治疗以耗尽肠道微生物群.
对认知功能和神经炎症标志物的评估.
对肠道微生物群组成的分析,重点是Akkermansia muciniphila (AKK).
使用抗体和重组蛋白质对TNF-α通路的研究.

主要成果:

在老年小鼠中,KF-8改善了与年龄相关的特征和认知缺陷.
KF-8重新塑造了肠道微生物群,特别是稳定了阿克尔曼西亚菌 (AKK).
在血液和海马体中,KF-8和AKK协同减弱了促炎途径,特别是TNF-α.
接受KF-8的抗生素治疗的小鼠表现出神经炎症和认知衰退,表明微生物群的依赖.
TNF-α抗体模仿了KF-8的益处,而TNF-α重组蛋白则否定了它们,突出了TNF-α的关键作用.

结论:

粉KF-8通过调节肠道微生物群和维持AKK水平,促进健康的衰老.
KF-8抑制TNF-α驱动的神经炎症,从而挽救老年小鼠的认知功能.
这些发现揭示了一种机制,KF-8通过肠道微生物群和TNF-α起作用,以对抗与年龄相关的认知衰退.

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