☆ 4.7 Article

Thalidomide (THD) alleviates radiation induced lung fibrosis (RILF) via down-regulation of TGF-beta/Smad3 signaling pathway in an Nrf2-dependent manner

FREE RADICAL BIOLOGY AND MEDICINE (2018)

Journal

FREE RADICAL BIOLOGY AND MEDICINE

Volume 129, Issue -, Pages 446-453

Publisher

ELSEVIER SCIENCE INC

DOI: 10.1016/j.freeradbiomed.2018.10.423

Keywords

Radiation-induced lung fibrosis; Thalidomide; TGF-beta/Smad3 signaling pathway; Nrf2; Mice

Categories

Biochemistry & Molecular Biology Endocrinology & Metabolism

Funding

Natural Science Foundation of Ningxia Province [NZ17144]
National Natural Science Foundation of China [81460477]
First-Class Discipline Construction Founded Project of NingXia Medical University
School of Clinical Medicine [NXYLXK2017A05]

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Abstract

Radiation-induced lung fibrosis (RILF) is a complication of radiotherapy in thoracic cancer patients. Thalidomide (THD) has a therapeutic effect on fibrotic and inflammatory disorders. The purpose of the current study was to investigate the therapeutic effect of THD on RILF in mice and better understand the underlying regulatory mechanisms of the therapeutic effect. We found that THD mitigated the fibrosis caused by irradiation in mice. The action of THD on RILF was related to the elevation of low levels reactive oxygen species (ROS), which inhibited the transforming growth factor-beta (TGF-beta)/Smad3 signaling pathway through activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Analysis of the therapeutic effect of THD using Nrf2-/- mouse model confirmed the role of Nrf2 in vivo. In addition, no radioprotective effect of THD on thoracic cancer cell lines was observed. In conclusion, these data showed that THD attenuated RILF in mice, which was mediated by Nrf2-dependent down-regulation of the TGF-beta/Smad3 pathway, suggesting THD as a potential novel agent for RILF prevention.

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