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• W2564130003 abstract "Intermittent hypoxia was a simulation of a high- altitude environment. Neuro-inflammation post brain ische- mia was considered as a vital impact which contributed to cognitive-functional deficit. The isoform of nitric oxide syn- thase (iNOS) was an inflammation factor secreted by microglias in neuro-inflammation. In this study, we established a high-altitude environment as the hypoxic condi- tion. Twenty mice were selected and randomized into a hyp- oxia 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." @default.
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• W2564130003 date "2015-01-01" @default.
• W2564130003 modified "2023-09-22" @default.
• W2564130003 title "Effectof Intermittent Hypoxiaon Neuro-functionalRecoveryPost Brain Ischemia in Mice" @default.
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• W2564130003 hasPublicationYear "2015" @default.
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