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Title 

Silibinin inhibits the fibrotic responses induced by cigarette smoke via suppression of TGF-β1/Smad 2/3 signaling

Authors 

J W KoN R ShinS H ParkIn Chul LeeJ M RyuH J KimY K ChoJ C KimI S Shin

Publisher 

Elsevier

Issue Date 

2017

Citation 

Food and Chemical Toxicology

Keywords 

Chronicobstructive pulmonary diseaseCigarette smokeCollagen depositionSilibininTGF-β1/Smad 2/3

Abstract 

Cigarette smoke (CS) is generally accepted as a major contributor to chronic obstructive pulmonary disease (COPD) which is characterized by chronic inflammation, fibrotic response, and airway obstruction. In this study, we investigated the preventive effects of silibinin, an active constitute of silymarin on CS and lipopolysaccharide (LPS) exposure-induced fibrotic response. Mice were exposed to CS for 1 h per day (8 cigarettes per day) for 4 weeks. On day 12 and 26, mice were treated with LPS intranasally. Silibinin (10 or 20 mg/kg) was administered orally 1 h before CS exposure. Silibinin markedly decreased the inflammatory cell count in the bronchoalveolar lavage fluid, and reduced levels of proinflammatory mediators. Silibinin suppressed CS + LPS-induced collagen deposition in lung tissue, as evidenced via immunohistochemistry and Masson's trichrome stain. Additionally, silibinin effectively inhibited CS + LPS-mediated expression of transforming growth factor-β1 (TGF-β1) and Smad 2/3 phosphorylation. Taken together, our data indicate that silibinin effectively inhibits the fibrotic response induced by CS + LPS exposure, possibly via suppression of TGF-β1/Smad 2/3 signaling, which results in reduced collagen deposition. These findings suggest that silibinin has therapeutic potential for the treatment of COPD.

ISSN 

0278-6915

Link 

http://dx.doi.org/10.1016/j.fct.2017.06.016

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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