Journal of Radiation Research and Radiation Proces ›› 2018, Vol. 36 ›› Issue (2): 20201-020201.doi: 10.11889/j.1000-3436.2018.rrj.36.020201

• RADIOBIOLOGY AND RADIOMEDICINE • Previous Articles     Next Articles

Effects and mechanism of CpG-ODN ameliorating radiation induced pulmonary fibrosis

ZHANG Chao1, GAO Fu2, CAI Jianming2   

  1. 1. Department of Radiotherapy, Lanzhou General Hospital of PLA, Lanzhou 730050, China;
    2. Faculty of Naval Medicine, The Second Military Medical University, Shanghai 200433, China
  • Received:2017-11-13 Revised:2018-01-15 Online:2018-04-20 Published:2018-04-19
  • Supported by:

    Supported by National Natural Science Foundation Youth Science Project of China (81501623)


The whole thorax of C57BL/6 female mice was irradiated to a single absorbed dose of 15 Gy. The formation of radiation-induced pulmonary fibrosis (RIPF) was assessed by lung index, Masson staining, Ashcroft score, and collagen synthesis for 20 weeks after irradiation. TGF-b1 was measured by ELISA assay, and the major proteins in TGF-b1/Smad-dependent pathway, including TGF-b, TbR, phosphor-Smad 2/3, and Smad 7, were detected by immunohistochemistry staining. The results showed that RIPF formation was significantly reduced when CpG-ODN was administered to mice irradiated. Expression of TGF-b1, a profibrotic cytokine, remained at a lower level. In TGF-b1-Smad-dependent pathways, TGF-b1, TbR, and phosphor-Smad 2/3 were downregulated, while Smad 7 was upregulated. This suggested that CpG-ODN prevented RIPF. The mechanism might be associated with a reduction of profibrogenic cytokine TGF-b1 and inhibition of the fibrosis-related downstream TGF-b1-Smad-dependent pathway.

Key words: Radiation induced pulmonary fibrosis, CpG-ODN, TGF-b1, Smad protein

CLC Number: 

  • R815