Abstract: Abstract: Objective　To explore the mechanism of Wnt 5a in the rat model of broncho-pulmonary dysplasia (BPD). Methods　(1) Cell level, A549 cells were divided into the two groups: the control group (carbon dioxide volume fraction 5%) and the BPD group (oxygen volume fraction 85%). After 48 hours of hyperoxia, the levels of pulmonary surfactant associated protein C (SPC), aquaporin 5 (AQP5) and Wnt 5a proteins were detected by Western blot assay, and the change of cell proliferation ability was detected by cell proliferation detection kit. (2) Animal level, newborn rats were randomly divided into the two groups: the control group (oxygen volume fraction 21%) and the BPD group (oxygen volume fraction 85%). After 7 days of hyperoxia, lung tissue was collected. HE staining was used to evaluate the pathological changes of BPD animal model, and Western blot assay was used to detect changes of Wnt 5a, SPC and AQP5 proteins in lung tissue. (3) Cell level, furthermore, Wnt 5a inhibitor was added to BPD cell model to verify the effect of Wnt 5a on SPC, AQP5 protein and cell proliferation. Results　Compared with the control group, the expression levels of SPC and AQP5 decreased, the expression of Wnt 5a increased, and the ability of cell proliferation decreased in BPD cell model. The expression levels of SPC and AQP5 protein were recovered after cells were treatment with Wnt 5a inhibitor, and the proliferation ability of A549 cells was also recovered. The number of alveoli decreased and the area of alveoli increased in the BPD group. The expression levels of SPC, AQP5 and Wnt 5a protein were consistent with the teand of BPD cell model. Conclusion　Wnt 5a is abnormally activated in the occurrence and development of BPD. In-depth exploration of the mechanism of Wnt 5a in BPD may provide new ideas for the prevention and treatment of BPD.

Key words: Wnt-5a protein, bronchopulmonary dysplasia, hyperoxia, A549 cells, aquaporin 5, pulmonary surfactant-associated protein C, rats, Sprague-Dawley