Neural Regeneration Research

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Involvement of the Wnt signaling pathway and cell apoptosis in the rat hippocampus following cerebral ischemia/reperfusion injury

Bin Liu, Jing Tang, Shiying Li, Yuqin Zhang, Yan Li, Xiaoliu Dong   

  1. First Department of Neurology, Affiliated Hospital of Hebei United University, Tangshan 063000, Hebei Province, China
  • Received:2012-07-26 Revised:2012-10-30 Online:2013-01-05 Published:2013-01-05
  • Contact: Bin Liu, First Department of Neurology, Affiliated Hospital of Hebei United University, Tangshan 063000, Hebei Province, China,liubintsh@126.com.
  • About author:Bin Liu★, Master, Chief physician, Professor.
  • Supported by:

    This study was supported by the Medical Research Key Program of Hebei Province, No. 20110531.

Abstract:

We investigated the role of the Wnt signaling pathway in cerebral ischemia/reperfusion injury by examining β-catenin and glycogen synthase kinase-3β protein expression in the rat hippocampal CA1 region following acute cerebral ischemia/reperfusion. Our results demonstrate that cell apoptosis increases in the CA1 region following ischemia/reperfusion. In addition, β-catenin and glycogen synthase kinase-3β protein expression gradually increases, peaking at 48 hours following reperfusion. Dickkopf-1 administration, after cerebral ischemia/reperfusion injury, results in decreased cell apoptosis, and β-catenin and glycogen synthase kinase-3β expression, in the CA1 region. This suggests that β-catenin and glycogen synthase kinase-3β, both components of the Wnt signaling pathway, participate in cell apoptosis following cerebral ischemia/reperfusion injury.

Key words: neural regeneration, brain injury, Dickkopf-1, Wnt signaling pathway, cell apoptosis, β-catenin, glycogen synthase kinase-3&beta, protein, cerebral ischemia/reperfusion injury, grant-supported paper, neuroregeneration