中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (15): 1460-1463.doi: 10.4103/1673-5374.139463

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

保护局灶性脑缺血再灌注损伤的可行策略:远隔缺血后适应

  

  • 收稿日期:2014-07-04 出版日期:2014-08-12 发布日期:2014-08-12
  • 基金资助:

    辽宁省科技厅自然基金(联合基金)(2013022021)

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.

摘要:

对脑组织等缺氧敏感器官,缺血后适应的程度难以把握。相比之下,远隔缺血后适应可以通过实施于非重要远端器官来保护一些对缺血敏感的器官。为此,实验设计了对局灶性脑缺血再灌注损伤模型大鼠采取动脉夹夹闭股动脉 10min,开放10 min,3个循环的远隔缺血后适应。发现远隔缺血后适应后,局灶性脑缺血再灌注损伤模型大鼠脑组织梗死比例明显下降,脑水肿减轻,缺血侧大脑皮质中炎症因子核因子κB表达显著降低,而抗凋亡蛋白Bcl-2表达水平显著升高。提示远隔缺血后适应可以减轻大鼠局灶性脑缺血再灌注产生的损伤,其保护作用的机制可能与抗细胞凋亡和降低损伤组织的炎症反应有关。

关键词: 神经再生, 远隔缺血后适应, 局灶性脑缺血, 神经保护, 细胞凋亡, 炎症, 脑损伤, 核因子κB, Bcl-2

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