Apigenin alleviates TGF-β1-induced nasal mucosa remodeling by inhibiting MAPK / NF-kB signaling pathways in chronic rhinosinusitis.

摘要: BACKGROUND Chronic rhinosinusitis is involved in tissue remodeling of nasal mucosa such as myofibroblast differentiation and extracellular matrix production. Apigenin (4',5,7-trihydroxyflavone) a bioflavonoid compound has anti-tissue characteristics. The aims this study were to evaluate the effect apigenin on TGF-β1-induced accumulation determine underlying mechanism. METHODS Nasal fibroblasts ex vivo inferior turbinate tissues stimulated with TGF-β1 or without apigenin. expression levels α-SMA, fibronectin collagen type I determined by real-time PCR, western blot immunocytochemical staining. Mitogen-activated protein kinase (MAPK) phosphorylation induced analysis. transcriptional activity NF-κB was measured luciferase assay. Migration effects evaluated wound scratch transwell migration Contractile gel contraction RESULTS fibronectin, significantly increased TGF-β1-stimulated fibroblasts. In fibroblasts, inhibited expressions I. Inhibitors MAPK (p-38, JNK) blocked suppressed activation treatment. also functional reducing contractile activities. CONCLUSIONS These results suggests possible use chronic therapeutic agent which can suppress mucosa.