Li Lin, Wang Hong-yang, Chen Bao-yuan, Zhang Pan-pan, Han Xiao-qing, Lei Jun-qi, Yang Lin
Department of Respiration, the Affiliated Hospital of Hebei United University, Tangshan 063000, China.
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2012 Feb;47(2):117-21.
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.
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.
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).
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.
根据间歇性缺氧机制建立不同程度及持续时间的睡眠呼吸暂停低通气综合征动物缺氧模型，观察c-fos蛋白及细胞凋亡情况，探讨神经系统损伤机制。
采用大鼠慢性间歇性缺氧模型，将雄性Wistar大鼠（n = 72）随机分为三组：5%慢性间歇性缺氧组（缺氧时氧体积分数降至5%）、10%慢性间歇性缺氧组（缺氧时氧体积分数降至10%）和对照组。分别在第2、4、6和8周检测三组海马细胞中c-fos蛋白水平及细胞凋亡情况。采用免疫组织化学方法检测海马细胞中c-fos蛋白表达，采用TUNEL法检测海马细胞凋亡。
在第2、4、6和8周时，慢性间歇性缺氧组的c-fos蛋白相对含量和凋亡指数均显著高于对照组（F分别为44.52、57.56、24.20和13.18，P < 0.05），且5%慢性间歇性缺氧组明显高于10%慢性间歇性缺氧组（P < 0.05）。两个慢性间歇性缺氧组中c-fos蛋白表达和凋亡指数因慢性间歇性缺氧的程度和持续时间不同而有所差异。随着暴露时间增加，c-fos蛋白表达和凋亡指数一般先升高，在第6周达到峰值，然后在第8周下降（P < 0.05）。而对照组在不同时间无变化（P > 0.05）。两个慢性间歇性缺氧组中c-fos蛋白相对含量与凋亡指数之间呈正相关（r分别为0.816和0.701，P < 0.01）。
中度和重度间歇性缺氧诱导海马中c-fos蛋白过度表达，导致神经细胞凋亡，可能在间歇性缺氧早期脑损伤机制中起重要作用。
