Background:Studies have shown that intermittent hypoxia mimics obstructive sleep apnea causing pulmonary inflammation,but the mechanism is not yet clear.TLR-4 is recognized proinflammatory factor,so the purpose of this article is research the function of TLR-4 in Pulmonary Inflammation Induced by Chronic intermittent hypoxia simulating obstructive sleep apnea.Methods: Male healthy Wistar rats were divided into 3 groups(eight in each group): normoxia control group(CG),intermittent hypoxia(IH),and TLR4 antagonist TAK242 treatment(3 mg/kg,daily),with exposure durations for 12 weeks and 16 weeks(HI).The morphological changes of lung tissue were determined with hematoxylin-eosin(HE)staining.The expressions of TLR-4 pathway in lung tissue were tested by Western blotting and RT-PCR.The levels of IL-6 and TNF-α in serum and lung tissue were detected by the enzyme linked immunosorbent assay(ELISA).The contents of SOD and MDA in lung tissue were detected by SOD and MDA kits,respectively.Results:After TAK242 treatment,the damage of lung tissue is extenuated,and the expression of TLR-4,MYD88,P65,IL-6,TNF-α,MDA and SOD are decreased.Intermittent hypoxic exposure caused alveolar expansion,thickening of alveolar septum,and fusion of adjacent alveoli into larger cysts under intermittent hypoxia in a time-dependent manner.Compared with the CG and HI group,the mean lining interval(MLI)become more thickened and the alveolar destruction index(DI)increased significantly in IH group.Conclusion: Chronic intermittent hypoxia causes pulmonary inflammatory response and the inflammatory pathway involved in TLR4 receptor may be one of the mechanisms that trigger lung inflammation.