title: Effect of intermittent hypoxia on neuro-functional recovery post brain ischemia in mice.
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.
authors.affiliation: Department of Emergency Medicine, Xixiang People's Hospital, Guangdong Medical College, Shenzhen, Guangdong, China.
authors.forename: Yanxiang
authors.initials: Y
authors.lastname: Qiao
authors.forename: Zhenfang
authors.initials: Z
authors.lastname: Liu
authors.forename: Xianliang
authors.initials: X
authors.lastname: Yan
authors.forename: Chuanming
authors.initials: C
authors.lastname: Luo
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism / Q000628:therapy*; D015687:Cell Hypoxia; D002460:Cell Line; D002478:Cells, Cultured; D003071:Cognition; D005947:Glucose / Q000172:deficiency; D006624:Hippocampus / Q000098:blood supply / Q000378:metabolism; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics / Q000378:metabolism; D019194:Ischemic Preconditioning; D008297:Male; D018782:Maze Learning; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism
chemical_list: C497443:Hif1a protein, mouse; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D052247:Nitric Oxide Synthase Type II; D005947:Glucose; D010100:Oxygen