中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (7): 727-734.doi: 10.4103/1673-5374.131577

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

电刺激小脑顶核影响脑缺血再灌注区神经元凋亡的机制

  

  • 收稿日期:2014-02-12 出版日期:2014-04-15 发布日期:2014-04-15
  • 基金资助:

    中国国家自然科学基金项目(30860291)

Neuronal apoptosis in cerebral ischemia/reperfusion area following electrical stimulation of fastigial nucleus

Jingli Liu, Jinpin Li, Yi Yang, Xiaoling Wang, Zhaoxia Zhang, Lei Zhang   

  1. Department of Neurology, the First Hospital Affiliated to Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China
  • Received:2014-02-12 Online:2014-04-15 Published:2014-04-15
  • Contact: Jingli Liu, Ph.D., Department of Neurology, the First Hospital Affiliated to Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China, lilicomet@163.com.

摘要:

作者既往研究发现电刺激大鼠的小脑顶核可减少脑梗死体积,而且其脑缺血再灌注区Ku70的表达增加,同时凋亡神经元减少,然而Ku70抗凋亡的具体分子途径尚未阐明。实验发现在建立脑缺血再灌注大鼠模型前24h电刺激小脑顶核,可使脑缺血再灌注大鼠脑梗死体积减小,脑缺血再灌注区Ku70表达增加,TUNEL阳性细胞数量减少。同时荧光双染显示,脑缺血再灌注大鼠脑缺血再灌注区中Ku70与TUNEL没有共定位,而Ku70与Bax部分共定位于胞浆。因此电刺激小脑顶核后脑缺血再灌注大鼠Ku70的抗细胞凋亡活性与细胞质中Ku70和Bax的共定位有关。

关键词: 神经再生, 脑损伤, 细胞凋亡, Ku70, Bax, 电刺激小脑顶核, 脑缺血再灌注损伤, DNA修复, NSFC

Abstract:

Previous studies have indicated that electrical stimulation of the cerebellar fastigial nucleus in rats may reduce brain infarct size, increase the expression of Ku70 in cerebral ischemia/reperfusion area, and decrease the number of apoptotic neurons. However, the anti-apoptotic mechanism of Ku70 remains unclear. In this study, fastigial nucleus stimulation was given to rats 24, 48, and 72 hours before cerebral ischemia/reperfusion injury. Results from the electrical stimulation group revealed that rats exhibited a reduction in brain infarct size, a significant increase in the expression of Ku70 in cerebral ischemia/reperfusion regions, and a decreased number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells. Double immunofluorescence staining revealed no co-localization of Ku70 with TUNEL-positive cells. However, Ku70 partly co-localized with Bax protein in the cytoplasm of rats with cerebral ischemia/reperfusion injury. These findings suggest an involvement of Ku70 with Bax in the cytoplasm of rats exposed to electrical stimulation of the cerebellar fastigial nucleus, and may thus provide an understanding into the anti-apoptotic activity of Ku70 in cerebral ischemia/reperfusion injury.

Key words: nerve regeneration, brain injury, apoptosis, Ku70, Bax, electrical stimulation, fastigial nucleus, cerebral ischemia/reperfusion injury, DNA repair, NSFC grant, neural regeneration