Abstract

Background and aims: Effects of different states of oxidative stress on fetal rat alveolar type IIepithelial cells in vitro and ROS-induced changes in Wnt signaling pathway expression. Aims: We aimed to investigate the effects of different states of oxidative stress on fetal rat alveolar type II epithelial cells (AEC II) cultured in vitro and reactive oxygen species (ROS)-induced changes in Wnt signaling pathway expression. Methods: Primary AEC II cultures were randomly divided into three oxidative damage groups: a high oxygen fraction (> 0.95) group (95% O2), a low oxygen fraction (0.4) group (40% O2) and a room air group (21% O2). Each group was exposed for 12, 24 and 48 h. Cell morphological changes were observed by inverted microscope, the cell survival rate was determined by MTT assay, and the apoptosis rate was determined by flow cytometry. Wnt5a gene expression was determined by RT-PCR and changes in non-phosphorylated β-catenin protein in the cell nucleus were determined by Western blot. Results: Compared with the room air group, the survival and apoptosis rates of the low oxygen fraction (0.4) group were not significantly different after 12 and 24 h, but the differences were significant after 48 h.The ROS concentration after 12 h in the high oxygen fraction (> 0.95) group was significantly higher than in the room air group, and continued to rise after 24 h. Conclusions: In conclusion: oxidative damage appeared after 48 h even with stimulation with low concentrations of oxygen (40%). The Wnt signaling pathway is an early regulatory factor involved in hyperoxia lung injury, and ROS can prematurely activate it.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.