Abstract
Radiation therapy has been used to treat over 70% of thoracic cancer; however, the method usually causes radiation pneumonitis. In the current study, we investigated the radioprotective effects of HSP27 inhibitor (J2) on radiation-induced lung inflammation in comparison to amifostine. In gross and histological findings, J2 treatment significantly inhibited immune cell infiltration in lung tissue, revealing anti-inflammatory potential of J2. Normal lung volume, evaluated by micro-CT analysis, in J2-treated mice was higher compared to that in irradiated mice. J2-treated mice reversed radiation-induced respiratory distress. However, amifostine did not show significant radioprotective effects in comparison to that of J2. In HSP27 transgenic mice, we observed increased immune cells recruitment and decreased volume of normal lung compared to wild type mice. Increased ROS production and oxidative stress after IR were down-regulated by J2 treatment, demonstrating antioxidant property of J2. The entire data of this study collectively showed that J2 may be an effective therapeutic agent for radiation-induced lung injury.
Original language | English |
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Article number | 4189 |
Journal | Scientific Reports |
Volume | 8 |
Issue number | 1 |
DOIs | |
State | Published - 1 Dec 2018 |
Bibliographical note
Funding Information:Funding for this study were provided by the following: Radiation Technology Research and Development Program (NRF-2015M2A2A7A03044831); Convergence of Conventional Medicine and Traditional Korean Medicine R&D program funded by Ministry of Health & Welfare through Korea Health Industry Development Institute (HI15C0214); Basic Science Research Program (NRF-2016R1A6A3A11932226, 2017R1D1A1B03027881) through National Research Foundation of Korea funded by Ministry of Education; Korea Institute of Radiological and Medical Sciences (KIRAMS) funded by Ministry of Science ICT (MSIT), Republic of Korea (1711045557;17 11045538;1711045554); and faculty research grant from Yonsei University College of Medicine (6–2016–0158).
Publisher Copyright:
© 2018 The Author(s).