In this study, we first isolated and cultured type II alveolar epithelial cells (AECs II) to establish a hyperoxia-induced AEC II model of BPD and then performed experiments with caffeine treatment, the A2AR antagonist ZM241385, the A2AR agonist CGS21680 and siRNA-A2AR interference to investigate the protective mechanism of caffeine against hyperoxia-induced lung injury in vitro. This evidence concerns the gene ADORA2A and bronchopulmonary dysplasia.