RT Journal Article SR Electronic T1 Sulforaphane attenuates lung fibrosis in bleomycin-induced pulmonary fibrosis via inhibition of TGF-β/Smad signaling JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP P3754 VO 44 IS Suppl 58 A1 Sun Young Kyung A1 You Jin Kim A1 Sang Min Lee A1 Sin Myung Kang A1 Sang Pyo Lee A1 Jeong-Woong Park A1 Sung Hwan Jeong YR 2014 UL http://erj.ersjournals.com/content/44/Suppl_58/P3754.abstract AB Sulforaphane(SFN) is a isothiocyanate that has chemoproventive, anti-inflammatory effects via NF-E2-related factor2 (Nrf2)-mediated induction of antioxidant/phase II enzymes. We evaluated the effects of sulforaphane on pulmonary fibrosis and profibrotic TGF-β/Smad signaling.Sulforaphane inhibited TGF-β-induced expression of fibronectin and collagen I in human pulmonary fibroblast cell lines (MRC-5 cells). Sulforaphane suppressed TGF-β-induced phosphorylation of Smad2/3. C57BL/6 male-gender mice in each group (control, BLM, BLM+SFN) were treated with BLM or SFN for 4 weeks. And then mice lungs were analyzed with histology (H&E, trichrome stain), western blot for TGF-β, fibronectin. The histological changes demonstrated that BLM instillation induced severe destruction of lung structure and accumulation of collagen in mice lungs. SFN treatment attenuated BLM-induced fibrotic lesions and collagen accumulation (hydroxyproline assay) in mice lungs. BLM increased TGF-β and fibronectin protein expression in lung tissues which was downregulated by SFN treatment.These findings suggest SFN treatment attenuates pulmonary fibrosis via inhibition of TGF-β/Smad signaling.