中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (2): 244-252.doi: 10.4103/1673-5374.346542

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

蛛网膜下腔出血后神经细胞凋亡的机制、介质及潜在的治疗靶点

  

  • 出版日期:2023-02-15 发布日期:2022-08-05

The mechanism and relevant mediators associated with neuronal apoptosis and potential therapeutic targets in subarachnoid hemorrhage

Qi Tian, Sheng Liu, Shou-Meng Han, Wei Zhang, Xian-Yao Qin, Jun-Hui Chen, Cheng-Li Liu, Yu-Jia Guo, Ming-Chang Li*    

  1. Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China
  • Online:2023-02-15 Published:2022-08-05
  • Contact: Ming-Chang Li, PhD, mingcli@whu.edu.cn.
  • Supported by:
    This study was supported by the National Natural Science Foundation of China, Nos. 81971870, 82172173 (both to MCL).

摘要: https://orcid.org/0000-0003-4019-8886 (Ming-Chang Li)

Abstract: blood-brain barrier; mechanism; mediators; neuronal apoptosis; pathways; subarachnoid hemorrhage; targets; treatmentSubarachnoid hemorrhage (SAH) is a dominant cause of death and disability worldwide. A sharp increase in intracranial pressure after SAH leads to a reduction in cerebral perfusion and insufficient blood supply for neurons, which subsequently promotes a series of pathophysiological responses leading to neuronal death. Many previous experimental studies have reported that excitotoxicity, mitochondrial death pathways, the release of free radicals, protein misfolding, apoptosis, necrosis, autophagy, and inflammation are involved solely or in combination in this disorder. Among them, irreversible neuronal apoptosis plays a key role in both short- and long-term prognoses after SAH. Neuronal apoptosis occurs through multiple pathways including extrinsic, mitochondrial, endoplasmic reticulum, p53 and oxidative stress. Meanwhile, a large number of blood contents enter the subarachnoid space after SAH, and the secondary metabolites, including oxygenated hemoglobin and heme, further aggravate the destruction of the blood-brain barrier and vasogenic and cytotoxic brain edema, causing early brain injury and delayed cerebral ischemia, and ultimately increasing neuronal apoptosis. Even there is no clear and effective therapeutic strategy for SAH thus far, but by understanding apoptosis, we might excavate new ideas and approaches, as targeting the upstream and downstream molecules of apoptosis-related pathways shows promise in the treatment of SAH. In this review, we summarize the existing evidence on molecules and related drugs or molecules involved in the apoptotic pathway after SAH, which provides a possible target or new strategy for the treatment of SAH.

Key words: blood-brain barrier, mechanism, mediators, neuronal apoptosis, pathways, subarachnoid hemorrhage, targets, treatment