Kanamaru Hideki, Suzuki Hidenori
Department of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Japan.
Neural Regen Res. 2019 Jul;14(7):1138-1143. doi: 10.4103/1673-5374.251190.
Aneurysmal subarachnoid hemorrhage remains serious hemorrhagic stroke with high morbidities and mortalities. Aneurysm rupture causes arterial bleeding-induced mechanical brain tissue injuries and elevated intracranial pressure, followed by global cerebral ischemia. Post-subarachnoid hemorrhage ischemia, tissue injuries as well as extravasated blood components and the breakdown products activate microglia, astrocytes and Toll-like receptor 4, and disrupt blood-brain barrier associated with the induction of many inflammatory and other cascades. Once blood-brain barrier is disrupted, brain tissues are directly exposed to harmful blood contents and immune cells, which aggravate brain injuries furthermore. Blood-brain barrier disruption after subarachnoid hemorrhage may be developed by a variety of mechanisms including endothelial cell apoptosis and disruption of tight junction proteins. Many molecules and pathways have been reported to disrupt the blood-brain barrier after subarachnoid hemorrhage, but the exact mechanisms remain unclear. Multiple independent and/or interconnected signaling pathways may be involved in blood-brain barrier disruption after subarachnoid hemorrhage. This review provides recent understandings of the mechanisms and the potential therapeutic targets of blood-brain barrier disruption after subarachnoid hemorrhage.
动脉瘤性蛛网膜下腔出血仍然是一种严重的出血性中风，具有很高的发病率和死亡率。动脉瘤破裂导致动脉出血引起的机械性脑组织损伤和颅内压升高，随后出现全脑缺血。蛛网膜下腔出血后的缺血、组织损伤以及外渗的血液成分和分解产物会激活小胶质细胞、星形胶质细胞和Toll样受体4，并破坏血脑屏障，引发许多炎症和其他级联反应。一旦血脑屏障被破坏，脑组织就会直接暴露于有害的血液成分和免疫细胞中，从而进一步加重脑损伤。蛛网膜下腔出血后血脑屏障的破坏可能是由多种机制引起的，包括内皮细胞凋亡和紧密连接蛋白的破坏。许多分子和信号通路已被报道与蛛网膜下腔出血后血脑屏障的破坏有关，但确切机制仍不清楚。多个独立和/或相互关联的信号通路可能参与蛛网膜下腔出血后血脑屏障的破坏。本文综述了蛛网膜下腔出血后血脑屏障破坏的机制及潜在治疗靶点的最新研究进展。
