Inhibition of pre-B cell colony-enhancing factor attenuates inflammation induced by hyperoxia in EA.hy926 cells.

The aim of this study was to investigate the role of pre-B cell colony-enhancing factor (PBEF) in the pathogenesis of bronchopulmonary dysplasia (BPD) using an established cell model of BPD. For this purpose, EA.hy926 cell cultures were divided into 4 groups as follows: the air group as the blank control, the hyperoxia group, the hyperoxia plus PBEF siRNA group and the hyperoxia plus scramble siRNA group. Cell viability and the generation of reactive oxygen species (ROS) were determined using respective kits. Moreover, the protein and mRNA expression levels of PBEF, interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) were also detected by corresponding methods. Compared with the hyperoxia group, the ROS levels in the hyperoxia plus PBEF siRNA group were significantly reduced (P<0.01). The silencing of PBEF increased cell viability compared with the hyperoxia group. The protein and mRNA expression levels of PBEF, IL-8 and TNF-α were all decreased in the hyperoxia plus PBEF siRNA group compared with the hyperoxia group (P<0.01). Our study thus demonstrates that the inhibition of PBEF attenuates oxidative stress and inflammation induced by hyperoxia in EA.hy926 cells, suggesting that PBEF may be a potential diagnostic and therapeutic target, which may be used for the development of novel treatment strategies for BPD.