Therapeutic effects of fibroblast growth factor-10 on hyperoxia-induced bronchopulmonary dysplasia in neonatal mice.

The survival rate of preterm neonates increases significantly with the development of neonatal care and comprehensive treatment, but more and more high-risk preterm neonates suffer from bronchopulmonary dysplasia (BPD). Currently, there is no effective treatment for BPD, thus it is still a major cause of disability and mortality in neonates. Thus, it is imperative to investigate the pathogenesis and treatment of BPD in depth. Fibroblast growth factor-10 (FGF-10) is a paracrine growth factor binding its receptors (FGFR1 and FGFR2) to regulate a lot of biological processes. FGF-10, with mitotic and chemotactic activities, plays an important role in histogenesis during embryonic stage. It can prevent and attenuate mechanical or infection induced inflammation in lung. Results showed lung FGF-10 expression reduced significantly in neonatal mice with BPD, and exogenous FGF-10 was able to promote the growth of pulmonary mesenchymal stem cells and alveolar epithelial cells type II and reduce the expression of pro-inflammatory cytokines. We preliminarily explored the relationship between FGF-10 and NF-κB in this animal model and found FGF-10 could inhibit NF-κB p65 expression as a feedback. Thus, to investigate the protective effects of FGF-10 on hyperoxia induced BPD in neonatal mice will provide a new strategy for the treatment of BPD.