Abstract
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.
Highlights
Radiotherapy (RT) is a major cancer therapeutic modality
Since TGF-β1 is known to be an important factor for fibrotic responses, we examined whether α-lipoic acid (α-LA) inhibits the increase in TGF-β1 expression and secretion in mouse NIH-3T3 fibroblasts upon irradiation (10 Gy)
We found that α-LA has a therapeutic effect on the radiation-induced soft tissue fibrotic change
Summary
Radiotherapy (RT) is a major cancer therapeutic modality. More than 40% of cancer patients receive RT. Radiation-induced fibrosis (RIF), one of the most common late complications of high-dose RT [2] along with necrosis, develops within months or years of RT [1, 3]. Radiation-induced fibrosis (RIF) is characterized by excessive accumulation of extracellular matrix in skin and soft tissue, and the proliferation of fibroblasts is one of the most common late complications of radiation therapy. The screening of natural compounds to identify histone acetyltransferase (HAT) inhibitors led to the discovery of garcinol, curcumin, anacardic acid, and EGCG, which may have value in the prevention of cancer, inflammation, and fibrosis [19, 20]. We report that aLA prevents radiation-induced fibrosis in mice by inhibiting the transcriptional activity of NF-κB, especially through the inhibition of TGF- β1mediated histone acetyltransferase (HAT) activation
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