we identified a molecular effector mechanism of the lncRNA uc.375 in lung tissue of BPD using lncRNA microarray, bioinformatics, and functional studies. We found that uc.375 is mainly distributed in AEC II, and low expression in BPD mice AEC II. Silencing uc.375 promoted the apoptosis of MLE 12 cells, reduced their proliferation and differentiation, and promoted the apoptosis-related factor caspase 3, inhibited the expression of MLE 12 specific secretion SP-C, bcl2 and UCP2. On the contrary, after overexpressing uc.375, the opposite results were obtained. Silencing uc.375 while silencing FoxA1 inhibited MLE 12 apoptosis, promoted their proliferation, inhibited apoptosis-related factor caspase3, and promoted the expression of MLE 12-specific secretions SP-C , bcl2 and UCP2. On the contrary, overexpression of uc.375 and FoxA1 at the same time, the result is opposite. uc.375 negatively regulates FoxA1 expression, affects alveolar development, and plays an important role in the occurrence and development of BPD. In summary, this study clarified the exact mechanism of uc.375 in the occurrence and development of BPD. we identified that it may provide a new molecular target for the prevention and treatment of BPD.