Effect of chronic intermittent hypoxia on the expression of fractalkine in rat liver

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 P0.01); compared with the 5% CIH group, the hepatic steatosis and inflammatory activity in the 5% CIH+RH group were dramatically reduced(P0.01). 2) Compared with the control group, the fractalkine expression in the 5% CIH and 5% CIH+RH groups was increased(both P0.01). The fractalkine expression in the 5% CIH+RH group was dramatically downregulated compared with that in the 5% CIH group(P0.01). Conclusion: CIH can induce liver injury and high fractalkine expression in rat liver tissues.