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): 2885-2894.doi: 10.3969/j.issn.1673-5374.2013.31.001

• 原著:脑损伤修复保护与再生 •    下一篇

常压高氧修复脑缺血损伤

  

  • 收稿日期:2013-04-02 修回日期:2013-09-16 出版日期:2013-11-05 发布日期:2013-11-05

Normobaric oxygen for cerebral ischemic injury

Chunhua Chen, Haimeng Cui, Zihe Li, Ruifeng Wang, Changman Zhou   

  1. Department of Anatomy and Histoembryology, Peking University Health Science Center, Beijing 100191, China
  • Received:2013-04-02 Revised:2013-09-16 Online:2013-11-05 Published:2013-11-05
  • Contact: Changman Zhou, Ph.D., Professor, Department of Anatomy and Histoembryology, Peking University Health Science Center, Beijing 100191, China, changmanzhou@ hotmail.com. Chunhua Chen, Department of Anatomy and Histoembryology, Peking University Health Science Center, Beijing 100191, China, cch@bjmu.edu.cn.
  • About author:Chunhua Chen, M.D., Ph.D.

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摘要：

研究表明吸入氧气可以增加脑缺血再灌注损伤时的组织氧供，保护受损神经细胞。但高压高氧可能会加重氧化应激反应，而常压高氧也能对缺血缺氧性疾病产生治疗作用。实验连续6d使大鼠吸入常压高氧（95%O2）后，以线栓法建立局灶性脑缺血模型。尼氏及TTC染色显示，常压高氧预处理使脑缺血大鼠大脑皮质神经元病理损伤减轻，梗死体积减小，免疫组化染色及Western blot检测结果显示缺血侧大脑组织中半暗带中缺氧诱导因子1及其调节的下游基因血管内皮生长因子，促红细胞生成素及Notch1的表达增加，行为学检测也证实大鼠神经缺损评分增加。在常压高氧前1h给大鼠腹腔注射缺氧诱导因子抑制剂2ME2可以抑制常压高氧的保护作用。由此推测常压高氧预处理可能通过活化缺氧诱导因子1α-Notch信号而达到预防局灶性脑缺血损伤的作用。

关键词: 神经再生, 脑损伤, 常压高氧, 脑缺血, 局灶性脑缺血, 血脑屏障, 缺氧诱导因子1α, Notch1, 缺氧诱导因子1-Notch信号通路, 基金资助文章

Abstract:

Oxygen inhalation has been shown to increase oxygen supply to tissues after cerebral ischemia/ reperfusion injury, protecting injured neural cells. However, hyperbaric oxygen may aggravate oxi-dative stress. By contrast, normobaric oxygen has the rapid and non-invasive characteristics and may have therapeutic effects on ischemic/hypoxic disease. Rats inhaled normobaric oxygen (95% O2) for 6 consecutive days, and then a rat model of focal cerebral ischemia was established. Nissl and 2,3,5-triphenyltetrazolium chloride (TTC) staining revealed that normobaric oxygen pretreat-ment improved neurological deficits and reduced infarct volume. Immunohistochemical staining and western blot assay revealed that the expression of hypoxia-inducible factor-1α, Notch-1, vascular endothelial growth factor and erythropoietin were increased. Behavioral studies also verified that neurological deficit scores increased. The hypoxia-inducible factor inhibitor 2-methoxyestradiol treatment at 1 hour before administration of normobaric oxygen could suppress the protective effect of normobaric oxygen. Given these observations, normobaric oxygen pretreatment may alleviate cerebral ischemic injury via the hypoxia-inducible factor signal pathway.