Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (15): 1460-1463.doi: 10.4103/1673-5374.139463

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A feasible strategy for focal cerebral ischemia-reperfusion injury: remote ischemic postconditioning

Qiang Liu 1, 2, Shengnian Zhou 1, Yaodong Wang 3, Fang Qi 2, Yuan Song 2, Siwei Long 2   

  1. 1 Department of Neurology, Qilu Hospital of Shandong University, Brain Science Research Institute of Shandong University, Jinan, Shandong Province, China
    2 Department of Neurology, Third Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China
    3 Department of Neurosurgery, Third Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning Province, China
  • Received:2014-07-04 Online:2014-08-12 Published:2014-08-12
  • Contact: Shengnian Zhou, M.D., Department of Neurology, Qilu Hospital of Shandong University, Brain Science Research Institute of Shandong University, No. 107 Wenhuaxi Road, Jinan 250012, Shandong Province, China, zhoushengnian126@126.com.
  • Supported by:

    This study was supported by the Natural Science Foundation (Joint Fund) of Liaoning Provincial Science and Technology Department, No. 2013022021.

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Abstract:

It is difficult to control the degree of ischemic postconditioning in the brain and other ischemia-sensitive organs. Remote ischemic postconditioning could protect some ischemia-sensitive organs through measures on terminal organs. In this study, a focal cerebral ischemia-reperfusion injury model was established using three cycles of remote ischemic postconditioning, each cycle consisted of 10-minute occlusion of the femoral artery and 10-minute opening. The results showed that, remote ischemic postconditioning significantly decreased the percentage of the infarct area and attenuated brain edema. In addition, inflammatory nuclear factor-κB expression was significantly lower, while anti-apoptotic Bcl-2 expression was significantly elevated in the cerebral cortex on the ischemic side. Our findings indicate that remote ischemic postconditioning attenuates focal cerebral ischemia/reperfusion injury, and that the neuroprotective mechanism is mediated by an anti-apoptotic effect and reduction of the inflammatory response.

Key words: nerve regeneration, remote ischemic postconditioning, focal cerebral ischemia, neuroprotection, apoptosis, inflammation, brain injury, nuclear factor-κB, Bcl-2, neural regeneration