中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (4): 641-645.doi: 10.4103/1673-5374.180751

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

缺血后处理上调酸敏感离子通道2a表达对缺血性脑损伤的神经保护

  

  • 收稿日期:2016-03-20 出版日期:2016-04-30 发布日期:2016-04-30

Ischemic postconditioning protects against ischemic brain injury by up-regulation of acid-sensing ion channel 2a

1 Department of Neurosurgery, General Hospital of Tibet Military Area Command, Lasa, China
2 Department of Neurosurgery, Southwest Hospital of Third Military Medical University, Chongqing, China   

  1. 1 Department of Neurosurgery, General Hospital of Tibet Military Area Command, Lasa, China
    2 Department of Neurosurgery, Southwest Hospital of Third Military Medical University, Chongqing, China
  • Received:2016-03-20 Online:2016-04-30 Published:2016-04-30
  • Contact: Hua Feng, M.D., fenghua9890@126.com.

摘要:

脑缺血后处理可使脑组织对缺血产生耐受,进而缓解致死性缺血所导致的损伤,但机制尚不十分清楚。为此,我们对全脑缺血模型大鼠采用血管阻断法进行缺血后处理:缺血2 h拔除线栓后立即夹闭双侧颈总动脉,阻断双侧颈总动脉血流10 s后再灌注10 s,循环6次。结果发现,缺血后处理使脑缺血大鼠海马CA1区神经元受损减轻,酸敏感离子通道2a基因和蛋白表达明显升高,证实缺血后处理可明显上调缺血性脑损伤海马区酸敏感离子通道2a的表达,使其在缺血耐受中起重要作用,以此发挥保护神经元损伤的作用。

orcid: 0000-0002-3605-7354 (Hua Feng)

关键词: 神经再生, 脑损伤, 缺血性脑损伤, 酸敏感离子通道, 神经保护, 缺血后处理, 神经保护, 蛋白表达, 神经元密度, 缺血耐受, 分子机制, 基因表达

Abstract:

Ischemic postconditioning renders brain tissue tolerant to brain ischemia, thereby alleviating ischemic brain injury. However, the exact
mechanism of action is still unclear. In this study, a rat model of global brain ischemia was subjected to ischemic postconditioning treatment
using the vessel occlusion method. After 2 hours of ischemia, the bilateral common carotid arteries were blocked immediately for
10 seconds and then perfused for 10 seconds. This procedure was repeated six times. Ischemic postconditioning was found to mitigate
hippocampal CA1 neuronal damage in rats with brain ischemia, and up-regulate acid-sensing ion channel 2a expression at the mRNA and
protein level. These findings suggest that ischemic postconditioning up-regulates acid-sensing ion channel 2a expression in the rat hippocampus
after global brain ischemia, which promotes neuronal tolerance to ischemic brain injury.

Key words: neural regeneration, brain injury, ischemic brain injury, acid-sensing ion channels, neuroprotection, ischemic postconditioning, neuroprotection, protein expression, neuronal density, ischemic tolerance, molecular mechanism, gene expression, nerve regeneration