Abstract
Objective: There is an increasing incidence of bronchopulmonary dysplasia (BDP) in preterm infants in China, which is the key issue affecting their survival rate and life quality. This study was performed to better understand the mechanism of protective effect of celecoxib on hyperoxia induced injury.Methods: Hyperoxia BPD model was established using newborn Sprague-Dawley (SD) rats exposed to high O2 level (85%). Celecoxib treatment was also conducted. Histology of lung tissue samples were analyzed. Functional studies were systematically performed using the lung tissues and A549 cells.Results: Hyperoxia disrupted lung development in SD rats. Celecoxib alleviated the damaged lung development. NF-κB and Aquaporin (AQP) 1 were identified as the pathways in the hyperoxia-induced lung injury. We have shown that hyperoxia activated NF-κB pathway through increased nucleus translocation and repressed AQP1 expression. On the contrary, celecoxib inhibited NF-κB phosphorylation and nucleus translocation and increased AQP1 expression through inhibiting COX2 activity. Additionally, celecoxib also rescued apoptosis induced by hyperoxia.Conclusion: Our study identified NF-κB and AQP1 as the pathways in the hyperoxia-induced lung injury in the hyperoxia BPD model SD rats and it provided a better understanding of the protective effect of celecoxib. It suggests NF-κB and AQP1 may be as potential targets for treating newborns with BPD.
Highlights
In recent years, the survival rate of preterm infants has been increasing with the advance of medical technology
We demonstrated that celecoxib alleviated the lung injury and rescued alveolar apoptosis in detail through inhibiting COX2, suppressing NFκB activation and increasing AQP1 expression, which presents a novel signaling pathway as therapeutic target
Celecoxib Improved Lung Development Disrupted by Hyperoxia in the Experimental Animal Model of BPD
Summary
The survival rate of preterm infants has been increasing with the advance of medical technology. There has been a rise of the incidence of bronchopulmonary dysplasia (BDP) in preterm infants who always require respiratory support, which became the key issue affecting their survival rate and life quality [1]. Hyperoxia exposure in premature infants results in apoptosis, arrested septation and inflammation, which eventually leads to the development of BPD [2, 3]. The treatment of BPD includes prenatal steroids, non-steroidal medicine and stem cell therapy [4]. There has been little research on the Non-Steroidal Anti-inflammatory Drug (NSAID) as a preventative and reparative treatment for BPD. Protection of Celecoxib on Hyperoxia-Induced Lung Injury
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