中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (1): 153-158.doi: 10.4103/1673-5374.150725

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

揭示亚低温抑制缺血再灌注损伤神经元凋亡的途径

  

  • 收稿日期:2014-10-12 出版日期:2015-01-15 发布日期:2015-01-15

The pathways by which mild hypothermia inhibits neuronal apoptosis following ischemia/reperfusion injury

Chun Luo 1, 2, Su-yue Pan 1, *   

  1. 1 Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China
    2 Department of Neurology, Guangxi Minzu Hospital, Nanning, Guangxi Zhuang Autonomous Region, China
  • Received:2014-10-12 Online:2015-01-15 Published:2015-01-15
  • Contact: Su-yue Pan, pansuyue82@126.com.

摘要:

已有研究证实亚低温有神经保护作用,且通过降低caspase-3表达可抑制缺血再灌注损伤内皮细胞凋亡。由此,作者设计了亚低温对氧糖剥夺模拟缺血再灌注神经元模型神经保护的验证实验。结果显示,亚低温干预明显减少了神经元凋亡数量、降低了促凋亡蛋白Bax的表达,提高了线粒体膜电位,且其抗凋亡作用最明显的时间段为6-12h。结果揭示了亚低温干预通过线粒体凋亡途径,抑制缺血再灌注神经元凋亡,且最佳作用时间窗为损伤后6-12h。

关键词: 神经再生, 亚低温, 氧糖剥夺, 细胞凋亡, 神经元, 线粒体膜电位, Bax, 缺血再灌注

Abstract:

Several studies have demonstrated that mild hypothermia exhibits a neuroprotective role and it can inhibit endothelial cell apoptosis following ischemia/reperfusion injury by decreasing casp-ase-3 expression. It is hypothesized that mild hypothermia exhibits neuroprotective effects on neurons exposed to ischemia/reperfusion condition produced by oxygen-glucose deprivation. Mild hypothermia significantly reduced the number of apoptotic neurons, decreased the expression of pro-apoptotic protein Bax and increased mitochondrial membrane potential, with the peak of anti-apoptotic effect appearing between 6 and 12 hours after the injury. These findings indicate that mild hypothermia inhibits neuronal apoptosis following ischemia/reperfusion injury by protecting the mitochondria and that the effective time window is 6–12 hours after ischemia/reperfusion injury.

Key words: nerve regeneration, mild hypothermia, oxygen-glucose deprivation, cell apoptosis, neurons, mitochondrial membrane potential, Bax, ischemia/reperfusion, neural regeneration