中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (31): 2895-2903.doi: 10.3969/j.issn.1673-5374.2013.31.002

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

低氧预适应促进急性脑梗死缺血半暗带血管新生

  

  • 收稿日期:2013-04-14 修回日期:2013-08-17 出版日期:2013-11-05 发布日期:2013-11-05
  • 基金资助:

    国家自然科学基金(30870854)；北京市自然科学基金重点项目(7111003)和山东省自然科学基金(ZR2010HM029)资助

Hypoxic preconditioning stimulates angiogenesis in ischemic penumbra after acute cerebral infarction

Sijie Li1, Yanbo Zhang2, Guo Shao3, Mingfeng Yang2, Jingzhong Niu2, Guowei Lv1, Xunming Ji1   

  1. 1 Institute of Hypoxic Medicine, Xuanwu Hospital, Capital Medical University, Beijing 100069, China
    2 Department of Neurology, Affiliated Hospital of Taishan Medical University, Taian 27100, Shandong Province, China
    3 Research Center of Biology and Medicine, Baotou Medical College, Baotou 014060, Inner Mongolia Autonomous Region, China
  • Received:2013-04-14 Revised:2013-08-17 Online:2013-11-05 Published:2013-11-05
  • Contact: Xunming Ji, M.D., Doctoral supervisor, Professor, Chief physician, Institute of Hypoxic Medicine, Xuanwu Hospital, Capital Medical University, Beijing 100069, China, jixm70@hotmail.com.
  • About author:Sijie Li, Master, Attending physician. Sijie Li and Yanbo Zhang contributed equally to this work.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 30870854; the Natural Science Foundation of Beijing, No. 7111003; and the Natural Science Foundation of Shandong Province, No. ZR2010HM029.

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摘要：

既往实验证实，低氧预适应对急性脑梗死具有保护作用，但具体保护机制不详。实验采用光化学法诱导Balb/c近交系小鼠脑皮质梗死模型，并于造模前30min对小鼠进行低氧预适应，从血管新生的角度探讨低氧预适应对急性脑梗死的保护机制。结果发现，脑梗死后24, 72h缺血半暗带区血管内皮生长因子和CD31表达明显增多，主要表达在脑内缺血半暗带区神经元和血管内皮细胞；低氧预适应可提高急性脑梗死小鼠缺血半暗带区血管内皮生长因子和CD31的表达。且血管内皮生长因子与CD31的表达成正相关。同时，低氧预适应可减少急性脑梗死小鼠的梗死灶体积，改善其神经功能缺损症状。可见低氧预适应对急性脑梗死具有保护作用，且此作用与增加急性脑梗死缺血半暗带区血管内皮生长因子和CD31表达，进一步促进血管新生有关。

关键词: 神经再生, 脑损伤, 低氧预适应, 急性脑梗死, 缺血半暗带, 血管内皮生长因子, CD31, 血管新生, 神经保护, 基金资助文章

Abstract:

Previous studies have demonstrated the protective effect of hypoxic preconditioning on acute cer-ebral infarction, but the mechanisms underlying this protection remain unclear. To investigate the protective mechanisms of hypoxic preconditioning in relation to its effects on angiogenesis, we in-duced a photochemical model of cerebral infarction in an inbred line of mice (BALB/c). Mice were then exposed to hypoxic preconditioning 30 minutes prior to model establishment. Results showed significantly increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra at 24 and 72 hours post infarction, mainly in neurons and vascular endothelial cells. Hy-Hypoxic preconditioning increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra and the expression of vascular endothelial growth factor was positively related to that of CD31. Moreover, hypoxic preconditioning reduced the infarct volume and improved neu-rological function in mice. These findings indicate that the protective role of hypoxic preconditioning in acute cerebral infarction may possibly be due to an increase in expression of vascular endothelial growth factor and CD31 in the ischemic penumbra, which promoted angiogenesis.

Key words: neural regeneration, brain injury, hypoxic preconditioning, acute cerebral infarction, ischemic penumbra, vascular endothelial growth factor, CD31, angiogenesis, neuroprotection, grants- supported paper, neuroregeneration