小胶质细胞
鼻腔给药
中枢神经系统
线粒体
医学
药物输送
药理学
神经科学
冲程(发动机)
机制(生物学)
细胞生物学
缺血
血脑屏障
输送系统
膜电位
神经系统
多发性硬化
全身给药
生物信息学
功能(生物学)
药品
体内
神经元
芬戈莫德
作者
Yue Yin,Zixuan Li,Weijie Shu,H. Y. Liu,Zihan Wang,Cong Fu,Yuanbo Zhu,X. Li,Yi Zhang,Bei Lv,Zixuan Wang,Qiaoqiao Zhao,Dan Liu,Lu Tang,Wei Wang
标识
DOI:10.1038/s41467-025-68024-5
摘要
Mitochondrial damage constitutes the central pathological mechanism of cerebral ischemia-reperfusion (I/R) injury. Targeted delivery of antioxidants to mitochondria and the phenotype polarization of glial cells holds great promise for effective treatment. However, the blood-brain barrier (BBB) remains a major obstacle, causing insufficient drug accumulation in neuronal mitochondria. Here, we develop a bioengineered nanolamellar system (MM@BPPF) by coating microglia-mitochondria hybrid biomembrane onto black phosphorus nanosheets (BP NSs) loaded with polymetformin (PolyMet) and fingolimod hydrochloride (FTY720). Microglia membrane facilitates inflammation-directed targeting to the injured brain regions, while mitochondria membrane confers homotypic targeting to mitochondria. Meanwhile, BP NSs, PolyMet, and FTY720 act sequentially to restore mitochondrial function of neuronal cells and modulate microglial polarization. Intranasal administration enables MM@BPPF to bypass the BBB, substantially improving brain-targeting efficiency. This work not only offers an innovative sequential targeting strategy for mitigating I/R injury but also presents a potential paradigm for treating other central nervous system disorders. Mitochondrial damage is a central pathological mechanism of cerebral ischemia-reperfusion injury. This study develops a bioengineered nanolamellar system to sequentially restore neuronal cell mitochondrial function and modulate microglial polarization to mitigate ischemia-reperfusion injury.
科研通智能强力驱动
Strongly Powered by AbleSci AI