创伤性脑损伤
非诺贝特
医学
脑水肿
药理学
氧化应激
神经保护
水肿
脑水肿
麻醉
血脑屏障
氧化磷酸化
神经学
内皮
中枢神经系统
冲程(发动机)
内皮功能障碍
炎症
缺血
内科学
病理
神经炎症
神经科学
作者
Qiyuan Feng,Yingwei Gao,Xiaokun Gu,Xinxin Zhao,Xinwen Liu,Zixuan Ma,Wenlan Qi,Zhenghui He,Yuhan Han,Jian Zhang,Wenye Wang,Zhifan Li,Daiwen Zhang,Jialin Huang,Yong Lin,Jiyuan Hui,Bayasgalan Onondari,Galbadrakh Erdenetsetseg,Qing Mao,Jiyao Jiang
出处
期刊:Redox biology
[Elsevier BV]
日期:2026-05-27
卷期号:94: 104240-104240
标识
DOI:10.1016/j.redox.2026.104240
摘要
Traumatic brain injury (TBI) frequently leads to brain edema, a life-threatening complication and a major cause of mortality and disability. Here, we report that fenofibrate (FFB), an agonist of the nuclear receptor peroxisome proliferator-activated receptor-α (PPARα), alleviates post-traumatic brain edema by enhancing blood-brain barrier (BBB) integrity in a mouse model of severe TBI. Mechanistic studies in cultured endothelial cells and endothelial-specific PPARα conditional knockout mice revealed that FFB activates PPARα, enhances mitochondrial oxidative phosphorylation (OXPHOS), and thereby reduces oxidative stress and endothelial cell apoptosis. These findings identify PPARα-dependent enhancement of energy metabolism in the brain endothelium as a promising therapeutic strategy for TBI-induced edema.
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