Research Papers:

Protective effect of α-lipoic acid against radiation-induced fibrosis in mice

Seung-Hee Ryu, Eun-Young Park, Sungmin Kwak, Seung-Ho Heo, Je-Won Ryu, Jin-hong Park, Kyung-Chul Choi and Sang-wook Lee _

PDF  |  HTML  |  Supplementary Files  |  How to cite  |  Order a Reprint

Oncotarget. 2016; 7:15554-15565. https://doi.org/10.18632/oncotarget.6952

Metrics: PDF 1029 views  |   HTML 1188 views  |   ?  


Seung-Hee Ryu1, Eun-Young Park1, Sungmin Kwak3,4, Seung-Ho Heo2, Je-Won Ryu2, Jin-hong Park1, Kyung-Chul Choi3,4,*, Sang-wook Lee1,*

1Department of Radiation Oncology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea

2Institute for Life Sciences, Asan Medical Center, Seoul, Korea

3Department of Biomedical Sciences and Department of Pharmacology, Cell Dysfunction Research Center (CDRC), University of Ulsan College of Medicine, Seoul, Korea

4Cell Dysfunction Research Center and Bio-Medical Institute of Technology (BMIT), University of Ulsan College of Medicine, Seoul, Korea

*These authors contributed equally to this work

Correspondence to:

Sang-wook Lee, e-mail: lsw@amc.seoul.kr

Kyung-Chul Choi, e-mail: choikc75@amc.seoul.kr

Keywords: radiation-induced fibrosis, α-lipoic acid, acetylation, NF-κB, PAI-1

Received: July 07, 2015     Accepted: December 05, 2015     Published: January 20, 2016


Radiation-induced fibrosis (RIF) is one of the most common late complications of radiation therapy. We found that α-lipoic acid (α-LA) effectively prevents RIF. In RIF a mouse model, leg contracture assay was used to test the in vivo efficacy of α-LA. α-LA suppressed the expression of pro-fibrotic genes after irradiation, both in vivo and in vitro, and inhibited the up-regulation of TGF-β1-mediated p300/CBP activity. Thus, α-LA prevents radiation-induced fibrosis (RIF) by inhibiting the transcriptional activity of NF-κB through inhibition of histone acetyltransferase activity. α-LA is a new therapeutic methods that can be used in the prevention-treatment of RIF.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 6952