目的 The aim of this research is to study the lung injury induced by chronic intermittent hypoxia(CIH) and to investigate the protective effect of angiotensin1-7 [Ang-(1-7)].方法 Male Sprague-Dawley rats(180～200g) were exposed to CIH for 21 days (intermittent hypoxia for 60 s with 21 ％ O2 and for 30 s with 10 ％ pure nitrogen, cyclically repeated for 8 h/day).We randomly assigned totally 24 male rats to a normoxia group (RA), a saline treated CIH group (C-S) and a Ang-(1-7) treated CIH group(C-A).Rats in the RA group were exposed to room-air stimulation, whereas rats in the other groups were exposed to CIH stimulation.Expression of TNF-α and IL-6 in lung tissue was studied with the use of immunohistochemistry.The levels of TNF-α and IL-6 in lung tissue were detected by enzyme-linked immunosorbent assay (ELISA) method and compared among all groups.Oxidative stress biomarkers were determined in the lung tissue.In addition, NADPH oxidase 4(Nox4) levels were determined by western blot.结果 More pulmonary pathological changes occurred in C-S group than the other groups.ELISA and immunohistochemical staining showed that concentration of TNF-α and IL-6 in lung tissue and serum observed in C-S group were significantly higher than in RA group.A similar trend showed in the C-A group, but the expression of TNF-a and IL-6 were lower than the the C-S group, there was a significant statistical significance (P＜0.01).The level of MDA and CAT were significantly elevated and SOD was decreased in the C-S group.A significant decrease in MDA and an increase in SOD and CAT were observed in C-A group relative to C-S group.The expression of Nox4 increased in C-S group and significantly reduced after the intervention of Ang-(1-7).结论 CIH causes enhancement of inflammation level and oxidative stress and results in pathological changes and structural damage of lung tissues.Treatment with Ang1-7 could reverse lung injury, at least partially, via inhibition of inflammation and oxidative stress.