中文摘要：

目的：利用大鼠模型观察慢性间歇低氧（chronic intermittenthypoxia，CIH）对肝的损伤以及对肝趋化因子fractalkine表达的影响，并探讨其可能的机制。方法：利用间歇低氧大鼠模型模拟阻塞性睡眠呼吸暂停低通气综合征（obstructive sleep apnea-hypopnea syndrome，OSAHS）的CIH的病理生理过程。30只雄性Spraque—Dawley大鼠随机分为5％慢性间歇低氧组、s％慢性间歇低氧复氧组和正常对照组，每组10只。5％慢性间歇低氧组给予间歇性低氧处理3周，低氧频率均为20次／h，每次循环180s，8h／d；s％慢性间歇低氧复氧组给予间歇性低氧处理3周，低氧频率均为20次／h，每次循环180s，8h／d，3周后继续正常气体环境饲养3周。处死大鼠后采用HE染色法观察各组大鼠肝组织病理改变，免疫组织化学法比较各组大鼠肝fractalkine的表达水平。结果：1）与正常对照组相比，5％慢性间歇低氧组和5％慢性间歇低氧复氧组大鼠肝脂肪变程度及炎症反应均增加（均P〈0．01）；s％慢性间歇低氧复氧组大鼠肝损伤较5％慢性间歇低氧组显著减轻（P〈0．01）。2）与正常对照组相比，5％慢性间歇低氧组和5％慢性间歇低氧复氧组大鼠肝组织fractalkine表达均显著增强（均P〈O．01）；5％慢性间歇低氧复氧组较5％慢性间歇低氧组显著减弱（P〈0．01）。结论：CIH可诱导大鼠肝组织损伤及大鼠肝组织趋化因子fractalkine表达增加。

英文摘要：

To investigate the effect of chronic intermittent hypoxia （CIH） on liver injury and the expression of fractalkine in rats and explore its possible mechanism. Methods： A CIH murine model was established to mimic the pathophysiology of obstructive sleep apnea-hypopnea syndrome （OSAHS） in humans. Thirty healthy male Spraque-Dawley rats were randomly assigned to 3 groups： a 5% CIH group, a 5% CIH＋RH （removal ofhypoxia） group and a control group （ 10 rats in each group）. The 5% CIH and 5% CIH＋RH groups were exposed to CIHfor 3 weeks, 8 h/d, and the frequency of hypoxia was 20 times/h. The 5% CIH＋RH group was then exposed to normal gaseous environment for another 3 weeks. After the experiment, liver sections were stained with hematoxylin-eosin （HE） and the liver pathology was observed. The expression of fractalkine in the liver tissues was detected by immunohistochemical method. with the control group, the hepatic steatosis and inflammatory activities in the 5% CIH and 5% CIH＋RH groups were more severe （all P〈0.01 ）; compared with the 5% CIH group, the hepatic steatosis and inflammatory activity in the S% CIH＋RH group were dramatically reduced （P〈0.01）. 2） Compared with the control group, the fractalkine expression in the 5% CIH and 5% CIH＋RH groups was increased （both P〈0.01）. The fractalkine expression in the 5% CIH＋RH group was dramatically downregulated compared with that in the 5% CIH group （V〈0.01）.Conclusion： CIH can induce liver injury and high fractalkine expression in rat liver tissues.