Neural Regeneration Research ›› 2013, Vol. 8 ›› Issue (31): 2885-2894.doi: 10.3969/j.issn.1673-5374.2013.31.001

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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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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.