Abstract
Aims & Objectives: The aim of this study is to investigate the effects of CGRP on DNA damage and cell death of alveolar epithelial type II cells (AEC II) exposed to 60% oxygen. Methods AEC II were isolated from 19–20 d fetal rat lung and exposed to air or 60% oxygen with CGRP or CGRP8-37. The cells were evaluated with SP-C immunofluorescence and ROS levels were detected by probing with DCFH-DA. Apoptosis rate and cell cycle of AEC II were analyzed by flow cytometry, and apoptosis was determined by immunblot of actived caspase 3. The DNA damage was confirmed by immunofluorescence of H2AX using High-Content Analysis. Results Results showed that the levels of ROS levels, apoptosis cell number and the expression of γH2AX were markedly increased in hyperoxia group compared with those in air group. Reversely, ROS levels, apoptosis cell number and the expression of γH2AX were significantly lower with a significant arrest of S and G2/M phases in CGRP/O2 group than in hyperoxia or CGRP8-37/O2 group. Conclusions We concluded that CGRP could protect lung epithelium cells against hyperoxic insult and up-regulation of CGRP is probably a potential approach to hyperoxic lung injury.
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 callDisclaimer: 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.
