Conclusions
These results suggest that delphinidin may inhibit TGF-β1-induced myofibroblast differentiation and ECM production through the MAPK/NF-κB signaling pathway in NPDFs.
Methods
NPDFs were stimulated with TGF-β1, with or without delphinidin, and the expression levels of α-SMA, fibronectin, and collagen type I were determined by RT-PCR, Western blot analysis, and collagen assay. The expression of α-SMA protein was measured by immunocytochemical staining. Mitogen-activated protein kinase and NF-κB activation induced by TGF-β1 were determined by Western blot analysis. The transcriptional activity of NF-κB was measured by luciferase assay.
Purpose
Nasal polyps are associated with chronic inflammation of the mucous membranes in the nose and paranasal sinuses and involved in extracellular matrix (ECM) accumulation. Delphinidin promotes ECM degradation in hepatitis and cardiac fibrosis. The aims of this study were to examine the inhibitory effect of delphinidin on TGF-β1-induced myofibroblast differentiation and ECM accumulation, and to determine the underlying mechanisms in nasal polyp-derived fibroblasts (NPDFs).
Results
The expression levels of α-SMA, fibronectin, and collagen type I increased in TGF-β1-stimulated NPDFs. In TGF-β1-induced NPDFs, delphinidin inhibited the expression of α-SMA, fibronectin, and collagen. Inhibitors of MAPK and NF-κB blocked the expression of α-SMA, fibronectin, and collagen type I. Delphinidin suppressed the activation of MAPK and NF-κB induced by TGF-β1 stimulation. Conclusions: These results suggest that delphinidin may inhibit TGF-β1-induced myofibroblast differentiation and ECM production through the MAPK/NF-κB signaling pathway in NPDFs.