Beijing Key Laboratory of Cancer Invasion and Metastasis Research, Department of Histology and Embryology, School of Basic Medical Sciences, Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing 100069, China.
Department of Neurology, The Second Hospital of Jiaxing City, Jiaxing, 314000 Zhejiang, China.
Oxid Med Cell Longev. 2022 Sep 2;2022:7762078. doi: 10.1155/2022/7762078. eCollection 2022.
The integrity of the blood-brain barrier (BBB) is mainly maintained by endothelial cells and basement membrane and could be regulated by pericytes, neurons, and glial cells including astrocytes, microglia, oligodendrocytes (OLs), and oligodendrocyte progenitor cells (OPCs). BBB damage is the main pathological basis of hemorrhage transformation (HT) and vasogenic edema after stroke. In addition, BBB damage-induced HT and vasogenic edema will aggravate the secondary brain tissue damage. Of note, after reperfusion, oxidative stress-initiated cascade plays a critical role in the BBB damage after acute ischemic stroke (AIS). Although endothelial cells are the target of oxidative stress, the role of glial cell-derived oxidative stress in BBB damage after AIS also should receive more attention. In the current review, we first introduce the physiology and pathophysiology of the BBB, then we summarize the possible mechanisms related to BBB damage after AIS. We aim to characterize the role of glial cell-derived oxidative stress in BBB damage after AIS and discuss the role of oxidative stress in astrocytes, microglia cells and oligodendrocytes in after AIS, respectively.
血脑屏障（BBB）的完整性主要由内皮细胞和基底膜维持，并可由周细胞、神经元以及神经胶质细胞（包括星形胶质细胞、小胶质细胞、少突胶质细胞和少突胶质前体细胞）来调节。BBB 损伤是中风后出血性转化（HT）和血管源性水肿的主要病理基础。此外，BBB 损伤引起的 HT 和血管源性水肿会加重继发性脑组织损伤。值得注意的是，在再灌注后，氧化应激引发的级联反应在急性缺血性脑卒中（AIS）后 BBB 损伤中起着关键作用。尽管内皮细胞是氧化应激的靶细胞，但星形胶质细胞来源的氧化应激在 AIS 后 BBB 损伤中的作用也应引起更多关注。在本综述中，我们首先介绍了 BBB 的生理学和病理生理学，然后总结了与 AIS 后 BBB 损伤相关的可能机制。我们旨在描述星形胶质细胞来源的氧化应激在 AIS 后 BBB 损伤中的作用，并分别讨论氧化应激在星形胶质细胞、小胶质细胞和少突胶质细胞中的作用。
