| Objective Bronchopulmonary dysplasia(BPD)is one of the most common respiratory diseases in premature infants,which seriously affects the long-term quality of life of them,and long-term inhalation of high concentration of oxygen is the main risk factor for BPD.Therefore,this experiment established the neonatal rat bronchopulmonary dysplasia model induced by hyperoxia,dynamically observed the pathological changes of the lung tissue and detected the expression of mi R-876-3p in the lung tissue of hyperoxia-induced neonatal rat BPD model,and analyzed the role of mi R-876-3p in the occurrence and development of BPD,so as to provide a theoretical basis for the pathogenesis,prevention and treatment of BPD.Methods Eighty newborn SD rats were randomly divided into hyperoxia group(n=40,Fi02=60%)and air group(n=40,Fi02=21%)within 2 hours after birth.The hyperoxia group was placed in a closed constant temperature oxygen chamber,the oxygen concentration was maintained at 60%,and the air group was exposed to atmospheric air.Lung tissue samples were taken on the 1st,7th,14 th and 21 st day after birth,and paraffin sections were stained with HE to observe the pathological changes of lung tissue.Radiant alveolar count(RAC)and alveolar septum thickness(AST)were performed,and quantitative real-time PCR(q RT-PCR)technique was used to detect the expression of mi R-876-3p.Results 1.Within 21 days after birth,with the prolongation of hyperoxia exposure time,the general growth of rats in the hyperoxia group was lower than that in the air group,and the body weight in the hyperoxia group was lower than that in the air group on 14 th and 21 st day(P<0.05).And gradually appeared slow response,low glossiness of coat,increased respiratory rate,cyanosis at the end of the toe,tilted head and so on.2.Compared with the air group,some alveoli in the hyperoxia group showed some pathological changes,such as fusion,decrease in number,increase in volume,uneven size,simplification of structure,rupture of alveolar septum,thickening and so on.It is suggested that the development of lung is blocked and lung injury.With the increase of age,the number of alveoli increased and the thickness of alveolar septum decreased in the air group,while the number of alveoli decreased and the thickness of the alveolar septum increased in the hyperoxia group.There were significant differences in the number of alveoli and the thickness of alveolar septum between the two groups on the14 th and 21 st day of the experiment(P<0.05).The pulmonary pathological changes in neonatal rat BPD model induced by hyperoxia were consistent with the pulmonary pathological characteristics of human "new" BPD.3.There was a difference in the expression of mi R-876-3p between the two groups.The expression of mi R-876-3p in the hyperoxia group decreased gradually and was significantly lower than that in the air group on the 7th and 14 th and 21st(P<0.05).In the air group,there was no significant change in the expression of mi R-876-3p from the 1st day to the 21 st day.Conclusion 1.In this study,a "new" BPD model of neonatal rats was successfully induced by hyperoxia;2.The expression of mi R-876-3p in the "new" BPD model of neonatal rat is decreased;3.The differential expression of mi R-876-3p may play a role in the occurrence and development of BPD. |
