| ObjectivesHyperoxia is very useful in neonatal medicine. however, long-time hyperoxia inhalation may cause lung injury. Lung injury caused by hyperoxia is a major contributing factor to the development of bronchopulmonary dysplasia (BPD). Long-time hyperoxia inhalation may create ROS, which can cause acute lung injury (ALI), and develops into lung fibrosis-bronchopulmonary dysplasis, consequently seriously influence neonate's life quality.Long-term exposure to oxygen of high concentration can induce bronchopulmonary dysplasia-like lesions in lung structure of mice, so hyperxia exposure model can be used in the bronchopulmonary dysplasia pathogenetic study. TGF-β1 is correlated with lung auxano and fibrosis and its role in hyperoxic lung injury in neonate isn't clear now. In this study, a neonatal mouse model of bronchopulmonary dysplasia was established, and dynamic changes of the lung tissue, and the expression level of TGF-β1 in the lung of neonatal mice exposed to the 60% concentration hyperoxia inhalation were observed. To explore:(1) the effect of 60% concentration hyperoxic exposure (60%) on pulmonary development and lung injury in neonatal mouse. (2) the role of TGF-β1 on a mouse model of bronchopulmonary dysplasia with moderate hyperoxic exposure.MethodsThirty clean female kunming(KM) mice which were less than 24 hours old were enrolled in this study. The mice were randomly divided into two groups:the normoxia group(FiO2 0.21, n=15) and experimental group(FiO2 O.60, n=15). At 2th day,7th day, 14th day,21th day and 28th day of exposure, body weight were recorded, pathological change of the lung tissue by light microscope and transmission electron microscope and radical alveoli count(RAC) were observed, and the expression levels of TGF-β1 protein were detected by immunohistochemistry.Results(1) Body weight:mice of experimental group had lower body weight than those of normoxia group 7 days later (P<0.05); (2) Lungmorphology:Compared with normoxia group, the arrest of lung development was accompanied by interstitial fibrosis. As for experimental group,lung development disorder can be seen at 7th day, and at 14th day lung of experimental group showed thinner walls of alveoli, simple alveolar structure, fewer and larger alveoli and at 21th day the normal structures of alveolar were disappeared; (3) Radical alveoli count(RAC):The RAC value was significantly decreased in the experimental group 7 days later (P<0.01); (4) Ultramicro-architecture of the alveolar epithelial typeⅡcell (AEC-Ⅱ):Swelled mitochondria(Mi) appeared at 2th day; at 7th day lamellar bodies(LB) began to evacuate and became worse at 14th day; mitochondria and lamellar bodies disappeared at 21th day; Mi, microvilli, and LB disappeared, karyopyknosis, caryolysis appeared at 28th day in the experimental group; (5) The expression level of TGF-β1:The expression level of TGF-β1 of experimental group increased continuously after 2th day compared with normoxia group (P<0.01).ConclusionLong-term exposure to oxygen of 60% concentration can lead to growth impediment and impaired lung development, which shares morphologic similarities to human bronchopulmonary dysplasia. Oxygen of 60% concentration can obviously increase the expression level of TGF-β1, and cause lung development arrest and lung fibrosis. Such results suggest that TGF-β1 play an important role in development and sustainmant of the pulmonary fibrosi (PF)... |
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