【摘要】 目的:利用大鼠模型观察慢性间歇低氧(chronic intermittent hypoxia,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、5%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;5%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180 s,8 h/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);5%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<0.01);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。更多还原

【Abstract】 Objective: 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 of hypoxia) group and a control group( 10 rats in each group). The 5% CIH and 5% CIH+RH groups were exposed to CIH for 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. Results: 1) Compared 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 5% 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(P<0.01). Conclusion: CIH can induce liver injury and high fractalkine expression in rat liver tissues.更多还原