中国神经再生研究(英文版) ›› 2019, Vol. 14 ›› Issue (7): 1138-1143.doi: 10.4103/1673-5374.251190

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

蛛网膜下腔出血后血脑屏障破坏的潜在治疗分子靶点

  

  • 出版日期:2019-07-15 发布日期:2019-07-15

Potential therapeutic molecular targets for bloodbrain barrier disruption after subarachnoid hemorrhage

Hideki Kanamaru, Hidenori Suzuki   

  1. Department of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Japan
  • Online:2019-07-15 Published:2019-07-15
  • Contact: Hidenori Suzuki, MD, PhD, suzuki02@clin.medic.mie-u.ac.jp
  • Supported by:

    This work was supported by a grant-in-aid for Scientific Research from Japan Society for the Promotion of Science (grant number: 17K10825) to HS.

摘要:

orcid: 0000-0002-8555-5448 (Hidenori Suzuki)

Abstract:

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.

Key words: blood-brain barrier, early brain injury, endothelial cell, subarachnoid hemorrhage, tight junction, inflammation, matricellular protein, Toll-like receptor 4