神经炎症
神经保护
伞形酮
肠道菌群
氧化应激
睡眠剥夺
犬尿氨酸途径
认知功能衰退
小胶质细胞
下调和上调
肠-脑轴
中枢神经系统
星形胶质细胞
贫困
化学
免疫系统
药理学
神经科学
生物
内分泌学
神经传递
睡眠(系统调用)
长时程增强
神经递质
快速眼动睡眠
犬尿氨酸
胆碱能的
内科学
免疫学
神经干细胞
病态行为
氧化磷酸化
医学
作者
Yuhan Jiang,Zhenhong Ni,Haochen Dai,Xiaohu Luo,Jiali Xing,Rui Wang,Xin Zhang
标识
DOI:10.1021/acs.jafc.5c07117
摘要
Sleep deprivation (SD) is a major contributor to cognitive impairment, often accompanied by central neuroinflammation and gut microbiota dysbiosis. The tryptophan (TRP) pathway, activated via indoleamine 2,3-dioxygenase (IDO), serves as a critical link between immune activation and neuronal damage. Umbelliferone (UMB), a naturally occurring coumarin compound, possesses anti-inflammatory, antioxidant, and microbiota-modulating properties. A cognitive impairment model induced by SD was established to evaluate the effects of UMB on the central nervous system. Our findings showed that UMB treatment significantly improved learning and memory performance in mice subjected to sleep deprivation, restored gut microbiota composition, and levels of short-chain fatty acids (SCFAs), inhibited IDO expression, and rebalanced TRP-KYN metabolism. Additionally, UMB reduced pro-inflammatory cell release and oxidative stress, suppressed astrocyte and microglial activation, and upregulated synaptic protein PSD-95. It suggested that UMB may exert neuroprotective effects by modulating the gut-brain metabolic axis and alleviating neuroinflammation and synaptic dysfunction.
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