Abstract
BackgroundChronic rhinosinusitis is involved in tissue remodeling of nasal mucosa such as nasal myofibroblast differentiation and extracellular matrix production. Apigenin (4’,5,7-trihydroxyflavone) is a bioflavonoid compound and has anti-tissue remodeling characteristics. The aims of this study were to evaluate the effect of apigenin on TGF-β1-induced myofibroblast differentiation and extracellular matrix accumulation and to determine the underlying mechanism.MethodsNasal fibroblasts and ex vivo nasal inferior turbinate tissues were stimulated with TGF-β1 with or without apigenin. The expression levels of α-SMA, fibronectin and collagen type I were determined by real-time PCR, western blot and immunocytochemical staining. Mitogen-activated protein kinase (MAPK) phosphorylation induced by TGF-β1 were determined by western blot analysis. The transcriptional activity of NF-κB was measured by luciferase assay. Migration effects of fibroblasts were evaluated by wound scratch and transwell migration assay. Contractile activity was determined by collagen gel contraction assay.ResultsThe expression levels of α-SMA, fibronectin, and collagen type I significantly increased in TGF-β1-stimulated nasal fibroblasts. In TGF-β1-stimulated nasal fibroblasts, apigenin inhibited the expressions of α-SMA, fibronectin, and collagen type I. Inhibitors of MAPK (p-38, JNK) and NF-κB blocked the expression of α-SMA, fibronectin and collagen type I. Apigenin suppressed the activation of MAPK (p-38, JNK) and NF-κB induced by TGF-β1 treatment. Apigenin also inhibited the functional activity of fibroblasts by reducing the migration and collagen contractile activities.ConclusionsThese results suggests the possible use of apigenin as a chronic rhinosinusitis therapeutic agent which can suppress tissue remodeling in nasal mucosa.
Highlights
Chronic rhinosinusitis (CRS) is a multifactorial inflammatory disease in nose and paranasal sinuses and lasts more than 12 weeks
The expression levels of α-SMA, fibronectin, and collagen type I significantly increased in transforming growth factor β1 (TGF-β1)-stimulated nasal fibroblasts
Apigenin suppressed the activation of Mitogen-activated protein kinase (MAPK) (p-38, JNK) and NF-κB induced by TGF-β1 treatment
Summary
Chronic rhinosinusitis (CRS) is a multifactorial inflammatory disease in nose and paranasal sinuses and lasts more than 12 weeks. 10% of the world’s population has this disease, and those infections are accompanied by symptoms such as nasal obstruction, congestion, discharge, and facial pain [1, 2]. Despite this disease being widespread, the pathogenesis of CRS is not fully understood. Chronic rhinosinusitis is involved in tissue remodeling of nasal mucosa such as nasal myofibroblast differentiation and extracellular matrix production. The aims of this study were to evaluate the effect of apigenin on TGF-β1-induced myofibroblast differentiation and extracellular matrix accumulation and to determine the underlying mechanism
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