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缺血性脑卒中后血脑屏障功能障碍与修复。

Blood-brain barrier dysfunction and recovery after ischemic stroke.

机构信息

Pittsburgh Institute of Brain Disorders & Recovery and Department of Neurology, University of Pittsburgh, Pittsburgh, PA 15213, USA; State Key Laboratory of Medical Neurobiology, Institute of Brain Sciences and Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.

Department of Neurosurgery, University of Michigan, Ann Arbor, MI 48109, USA.

出版信息

Prog Neurobiol. 2018 Apr-May;163-164:144-171. doi: 10.1016/j.pneurobio.2017.10.001. Epub 2017 Oct 5.

Abstract

The blood-brain barrier (BBB) plays a vital role in regulating the trafficking of fluid, solutes and cells at the blood-brain interface and maintaining the homeostatic microenvironment of the CNS. Under pathological conditions, such as ischemic stroke, the BBB can be disrupted, followed by the extravasation of blood components into the brain and compromise of normal neuronal function. This article reviews recent advances in our knowledge of the mechanisms underlying BBB dysfunction and recovery after ischemic stroke. CNS cells in the neurovascular unit, as well as blood-borne peripheral cells constantly modulate the BBB and influence its breakdown and repair after ischemic stroke. The involvement of stroke risk factors and comorbid conditions further complicate the pathogenesis of neurovascular injury by predisposing the BBB to anatomical and functional changes that can exacerbate BBB dysfunction. Emphasis is also given to the process of long-term structural and functional restoration of the BBB after ischemic injury. With the development of novel research tools, future research on the BBB is likely to reveal promising potential therapeutic targets for protecting the BBB and improving patient outcome after ischemic stroke.

摘要

血脑屏障(BBB)在调节血液-脑界面的液体、溶质和细胞的转运以及维持中枢神经系统的稳态微环境方面起着至关重要的作用。在病理条件下,如缺血性中风,BBB 可以被破坏,随后血液成分渗出到大脑并损害正常的神经元功能。本文综述了我们对缺血性中风后 BBB 功能障碍和恢复的机制的最新认识。神经血管单元中的中枢神经系统细胞以及血液来源的外周细胞不断调节 BBB,并影响其在缺血性中风后的破坏和修复。中风风险因素和合并症的参与通过使 BBB 易于发生解剖和功能变化,从而加重 BBB 功能障碍,进一步使神经血管损伤的发病机制复杂化。本文还强调了缺血性损伤后 BBB 的长期结构和功能恢复过程。随着新型研究工具的发展,对 BBB 的未来研究可能会揭示有希望的治疗靶点,以保护 BBB 并改善缺血性中风患者的预后。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/274e/5886838/ca1eb0324496/nihms913279f1.jpg

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