Benzyl Isothiocyanate Suppresses Myofibroblast Differentiation and Extracellular Matrix Production in TGF-β1–Induced Nasal Polyp Fibroblasts

Background and Objectives Benzyl isothiocyanate (BITC) is an effector molecule in many cruciferous vegetable defense systems with antioxidant, anti-tumor, and anti-inflammatory activity. In the present study, the effects of BITC on organ-cultured nasal polyps (NPs) and transforming growth factor (TGF)-β1-induced profibrotic responses in nasal polyp-derived fibroblasts (NPDFs) were evaluated, and the associated signaling pathways were explored.Materials and Method Organ-cultured NPs and NPDFs were obtained from patients with NPs. Organ-cultured NPs were treated with BITC (0 or 5 μM). The NPDFs were treated with TGF-β1 (1 ng/mL) in the presence or absence of BITC (1, 3, and 5 μM). The expression levels of Collagen-1 (Col-1) and α-smooth muscle actin (α-SMA) in organ-cultured NPs were measured by western blot analysis. The expression levels of Col-1, α-SMA, and phosphorylatedsmall mothers against decapentaplegic (Smad2 and Smad3) in NPDFs were also measured by western blot analysis. The contractile activity of the NPDFs was determined by a collagen gel contraction assay. Results BITC reduced α-SMA and Col-1 expression in organ-cultured NPs but did not show biologically meaningful cytotoxic effects in TGF-β1-stimulated NPDFs within the tested concentration range. In TGF-β1-stimulated NPDFs, BITC attenuated the expression of α-SMA and Col-1 and suppressed collagen gel contraction. BITC treatment was associated with decreased phosphorylation of Smad2 and Smad3.Conclusion These findings suggest that BITC may exert antifibrotic effects in TGF-β1-induced fibroblast activation and may serve as a potential modulator in fibrosis-dominant remodeling of NPs.