title: [Influence of different degrees of chronic intermittent hypoxia on c-fos protein and apoptosis in rats].
abstract: OBJECTIVE
  To establish different degrees and duration of animal hypoxia model of sleep apnea hypopnea syndrome according to the mechanism of intermittent hypoxia, to observe the effect of c-fos protein and apoptosis, and to explore the mechanism of nervous system injury.
  
  
  METHODS
  By using the model of chronic intermittent hypoxia in rats, male Wistar rats (n = 72) were randomly divided into three groups: 5% of chronic intermittent hypoxia group (the fraction of oxygen volume reduced to 5% under hypoxia), 10% of chronic intermittent hypoxia group (the fraction of oxygen volume reduced to 5% under hypoxia) and control group. The levels of on c-fos protein and apoptosis of hippocampal cell in three groups were detected at the 2nd, 4th, 6th and 8th week respectively. The expression of c-fos protein in hippocampal cell was detected by immunohistochemical method and the apoptosis of hippocampal cell was detected by TUNEL.
  
  
  RESULTS
  The relative quantity of c-fos protein and apoptotic index in CIH groups were significantly higher than that of the control group on the 2nd, 4th, 6th and 8th weeks (F were 44.52, 57.56, 24.20 and 13.18, P < 0.05), and these were higher obviously in 5% CIH group than that in 10% CIH group (P < 0.05). The expression of c-fos protein and apoptotic index in two CIH groups was different depending upon the different degree and duration of chronic intermittent hypoxia. With increased exposure time, the expression of c-fos protein and apoptotic index was high generally at first, peaked at 6th week, then down at 8th week (P < 0.05). While it in UC group was invariability in different time (P > 0.05). The correlation between the relative quantity of c-fos protein and apoptotic index in two CIH groups was positive (r were 0.816 and 0.701, P < 0.01).
  
  
  CONCLUSIONS
  Moderate and severe intermittent hypoxia induced the excessive expression of c-fos protein in hippocampus, caused nerve cell apoptosis, and may play an important role in the mechanism of early brain injury of intermittent hypoxia.
authors.affiliation: Department of Respiration, the Affiliated Hospital of Hebei United University, Tangshan 063000, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Li
authors.forename: Hong-yang
authors.initials: HY
authors.lastname: Wang
authors.forename: Bao-yuan
authors.initials: BY
authors.lastname: Chen
authors.forename: Pan-pan
authors.initials: PP
authors.lastname: Zhang
authors.forename: Xiao-qing
authors.initials: XQ
authors.lastname: Han
authors.forename: Jun-qi
authors.initials: JQ
authors.lastname: Lei
authors.forename: Lin
authors.initials: L
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism*; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D009474:Neurons / Q000378:metabolism; D018384:Oxidative Stress; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D020181:Sleep Apnea, Obstructive / Q000378:metabolism*
chemical_list: D016760:Proto-Oncogene Proteins c-fos