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Effect of Intermittent Hypoxia on Neuro-functional Recovery Post Brain Ischemia in Mice

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Abstract

Intermittent hypoxia was a simulation of a high-altitude environment. Neuro-inflammation post brain ischemia was considered as a vital impact which contributed to cognitive-functional deficit. The isoform of nitric oxide synthase (iNOS) was an inflammation factor secreted by microglias in neuro-inflammation. In this study, we established a high-altitude environment as the hypoxic condition. Twenty mice were selected and randomized into a hypoxia group (n = 10) or a normoxia group (n = 10) post three vessel occlusion-induced brain ischemia. An enhancement of cognitive-functional recovery was presented in the hypoxia group by survival neuron counting and revealed by the Morris water maze test. Meanwhile, a high level of hypoxia-inducable factor 1 (HIF-1) expression associated with a lower expression of iNOS was observed in the border between infarcts and normal tissue of the hippocampus in the hypoxia group. However, these phenomenons were blocked by HIF-1 inhibition. This suggested that the acceleration of cognitive-functional recovery induced by intermittent hypoxia may depend on HIF-1 activating. An imitation of the hypoxic condition with or without HIF-1 inhibition was operated on the BV-2 cell. A high level of HIF-1 expression associated with a lower-level expression of iNOS was performed in the hypoxic condition. These data suggested that intermittent hypoxia can accelerate cognitive function recovery through attenuating neuro-inflammation.

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Correspondence to Chuanming Luo.

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Qiao, Y., Liu, Z., Yan, X. et al. Effect of Intermittent Hypoxia on Neuro-functional Recovery Post Brain Ischemia in Mice. J Mol Neurosci 55, 923–930 (2015). https://doi.org/10.1007/s12031-014-0447-8

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  • DOI: https://doi.org/10.1007/s12031-014-0447-8

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