中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (11): 1122-1128.doi: 10.4103/1673-5374.135314

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

保护老年短暂性脑缺血后海马细胞凋亡的潜在作用靶点

  

  • 收稿日期:2014-05-05 出版日期:2014-06-12 发布日期:2014-06-12

Potential targets for protecting against hippocampal cell apoptosis after transient cerebral ischemia-reperfusion injury in aged rats

  • Received:2014-05-05 Online:2014-06-12 Published:2014-06-12
  • Contact: Zangong Zhou, Department of Anesthesiology, Affiliated Hospital of Qingdao University, Qingdao 266071, Shandong Province, China, zhzg70916@sohu.com.
  • Supported by:

    This study was supported by a grant from Ministry of Science and Technology of Qingdao City, No. 10-3-4-7-8-JCH.

Abstract:

Mitochondria play an important role in neuronal apoptosis caused by cerebral ischemia, and the role is mediated by the expression of mitochondrial proteins. This study investigated the involvement of mitochondrial proteins in hippocampal cell apoptosis after transient cerebral ischemia-reperfusion injury in aged rats using a comparative proteomics strategy. Our experimental results show that the aged rat brain is sensitive to ischemia-reperfusion injury and that transient ischemia led to cell apoptosis in the hippocampus and changes in memory and cognition of aged rats. Differential proteomics analysis suggested that this phenomenon may be mediated by mitochondrial proteins associated with energy metabolism and apoptosis in aged rats. This study provides potential drug targets for the treatment of transient cerebral ischemia-reperfusion injury.

Key words: nerve regeneration, cerebral ischemia, reperfusion injury, hippocampus, cognitive function, apoptosis, mitochondria, differential proteomics, rats, aged, neural regeneration

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