中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2012, Vol. 7 ›› Issue (19): 1507-1512.

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

Ischemic postconditioning enhances glycogen synthase kinase-3β expression and alleviates cerebral ischemia/reperfusion injury

  

  • 收稿日期:2011-12-30 修回日期:2012-05-07 出版日期:2012-07-05 发布日期:2012-07-05

Ischemic postconditioning enhances glycogen synthase kinase-3β expression and alleviates cerebral ischemia/reperfusion injury

Bo Zhao1, Wenwei Gao2, Jiabao Hou1, Yang Wu1, Zhongyuan Xia1   

  1. 1 Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
    2 Department of Intensive Care Unit, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
  • Received:2011-12-30 Revised:2012-05-07 Online:2012-07-05 Published:2012-07-05
  • Contact: Zhongyuan Xia, M.D., Professor, Chief physician, Doctoral supervisor, De-partment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China xiazhongyuan2005@yahoo. com.cn
  • About author:Bo Zhao★, Master, Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China Bo Zhao and Wenwei Gao contributed equally to this work.

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Abstract:

cerebral ischemia/reperfusion| glycogen synthase kinase-3β| ischemic postconditioning| ischemic preconditioning| apoptosis| neural regenerationThe present study established global brain ischemia using the four-vessel occlusion method. Following three rounds of reperfusion for 30 seconds, and occlusion for 10 seconds, followed by reperfusion for 48 hours, infarct area, the number of TUNEL-positive cells and Bcl-2 expression were significantly reduced. However, glycogen synthase kinase-3β activity, cortical Bax and caspase-3 expression significantly increased, similar to results following ischemic postconditioning. Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity, a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway, which reduces caspase-3 expression to protect the brain against ischemic injury.

Key words: cerebral ischemia/reperfusion, glycogen synthase kinase-3β, ischemic postconditioning, ischemic preconditioning, apoptosis, neural regeneration