Obstructive sleep apnea (OSA) is characterized by recurrent episodes of partial or complete interruption in breathing during sleep due to collapse or obstruction of the upper airway.Chronic intermittent hypoxia(CIH) is a major pathophysiologic character of OSA.There is growing evidence that CIH can induce systemic inflammation.In this study, we assessed the level of inflammation and the expression of nuclear factor kappa B(NF-κB),hypoxia inducible factor-1 α (HIF-1α) and matrix metalloproteinase-9(MMP-9) in the lung from rats subjected to CIH and hypothesized that re-oxygen could result in attenuation of lung inflammation.We developed a rat model of CIH to simulate the profile in OSA.Rats were randomly divided into three groups, CIH group, re-oxygen group and control group respectively.Histological changes of lung was examined and the degree of inflammation was evaluated.Expression of NF-κB protein, HIF-1α mRNA, and MMP-9 mRNA in the lung were measured.Severe inflammatory cells infiltration and inflammatory exudation were observed in the lungs of rats from CIH group.These pathological changes were partially attenuated by subsequent treatment of re-oxygen.The expression of NFκB protein was increased in the lungs of rats from CIH group, while decreased after re-oxygen.The expression of HIF-1α mRNA and MMP-9 mRNA was increased in the lungs of rats from CIH group, while decreased after re-oxygen.Exposure to CIH resulted in inflammation and elevated expression of NF-κB, HIF-1α and MMP9 in the lung.Re-oxygen could ameliorate CIH-induced lung inflammation and overexpression of NF-κB, HIF1α and MMP-9.The present findings may implicate the clinical relationship between OSA and lung injury and suggest therapeutic potential of re-oxygen for CIH-induced lung inflammation.