Open AccessPolydatin alleviated radiation‐induced lung injury through activation of Sirt3 and inhibition of epithelial–mesenchymal transition
Author(s) -
Cao Kun,
Lei Xiao,
Liu Hu,
Zhao Hainan,
Guo Jiaming,
Chen Yuanyuan,
Xu Yang,
Cheng Ying,
Liu Cong,
Cui Jianguo,
Li Bailong,
Cai Jianming,
Gao Fu,
Yang Yanyong
Publication year - 2017
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13230
Subject(s) - epithelial–mesenchymal transition , lung , inflammation , mesenchymal stem cell , fibrosis , cancer research , pulmonary fibrosis , medicine , pneumonitis , pathology , chemistry , immunology , cancer , metastasis
Radiation‐induced lung injury ( RILI ) is one of the most common and fatal complications of thoracic radiotherapy. It is characterized with two main features including early radiation pneumonitis and fibrosis in later phase. This study was to investigate the potential radioprotective effects of polydatin ( PD ), which was shown to exert anti‐inflammation and anti‐oxidative capacities in other diseases. In this study, we demonstrated that PD ‐mitigated acute inflammation and late fibrosis caused by irradiation. PD treatment inhibited TGF ‐β1‐Smad3 signalling pathway and epithelial–mesenchymal transition. Moreover, radiation‐induced imbalance of Th1/Th2 was also alleviated by PD treatment. Besides its free radical scavenging capacity, PD induced a huge increase of Sirt3 in culture cells and lung tissues. The level of Nrf2 and PGC 1α in lung tissues was also elevated. In conclusion, our data showed that PD attenuated radiation‐induced lung injury through inhibiting epithelial–mesenchymal transition and increased the expression of Sirt3, suggesting PD as a novel potential radioprotector for RILI .