Open AccessModerate hyperoxia plays a protective role in lung bronchial epithelial cells
Author(s) -
Shimiao Tang,
Siyu Sun,
Dongyang Zhang,
Dongyan Liu
Publication year - 2019
Publication title -
clinical and investigative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.391
H-Index - 47
eISSN - 1488-2353
pISSN - 0147-958X
DOI - 10.25011/cim.v42i4.33114
Subject(s) - hyperoxia , relb , apoptosis , andrology , western blot , tumor necrosis factor alpha , downregulation and upregulation , microbiology and biotechnology , biology , lung , immunology , medicine , chemistry , nfkb1 , biochemistry , transcription factor , gene
Purpose: Oxygen therapy is commonly used in clinical settings, but several problems may result from improper use. Oxygen poisoning involves the initiation of a series of inflammatory reactions. In this study, we compared the effects of moderate hyperoxia (40% O2) and extreme hyperoxia (85% O2) on pulmonary bronchial epithelial cells.
Methods: Normal human tracheobronchial epithelium (NHBE) cells were exposed to hyperoxia (40% and 85%) for 24 hours, and their survival rates were determined by the colorimetic assay, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide). The protein and mRNA levels of RelA, RelB, ASK1, TNF-α and secretory component (SC) were detected by immunohistochemical staining, western blot, and real-time polymerase chain reaction.
Results: The NHBE cell survival increased in the presence of moderate hyperoxia. RelA, RelB, ASK1, TNF-α and SC expressions were significantly higher in the 85% O2 group in comparison with the control group and the 40% O2 group. In the 40% O2 group, RelA, RelB, ASK1 and TNF-α were upregulated, but SC expression was not significantly different than that of the control group. However, compared with the 85% O2 group, SC expression was significantly lower in the 40% O2 group.
Conclusion: These results suggest that moderate hyperoxia promotes proliferation in NHBE cells and activates TNF-α and downstream ASK1. Then TNF-α activates NF-κB and SC to play a protective role.