FUCOXANTHIN INHIBITS MYOFIBROBLAST DIFFERENTIATION AND EXTRACELLULAR MATRIX PRODUCTION IN NASAL POLYP-DERIVED FIBROBLASTS VIA MODULATION OF SMAD-DEPENDENT AND SMAD-INDEPENDENT SIGNALING PATHWAYS

Fucoxanthin Inhibits Myofibroblast Differentiation and Extracellular Matrix Production in Nasal Polyp-Derived Fibroblasts via Modulation of Smad-Dependent and Smad-Independent Signaling Pathways

Fucoxanthin Inhibits Myofibroblast Differentiation and Extracellular Matrix Production in Nasal Polyp-Derived Fibroblasts via Modulation of Smad-Dependent and Smad-Independent Signaling Pathways

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Nasal polyps (NPs) are a multifactorial disorder associated with a chronic inflammatory state of the nasal mucosa.Fucoxanthin (Fx) is a characteristic orange carotenoid obtained from brown algae and has diverse immunological properties.The present study investigated whether Fx inhibits fibrosis-related effects in nasal polyp-derived fibroblasts (NPDFs) and elucidated the molecular signaling pathways involved.

The production of collagen miracle academy clothing type I (Col-1) was investigated in NP tissue via immunohistochemistry and western blot analysis.NPDFs were treated with transforming growth factor (TGF)-β1 (1 ng/mL) in the presence or absence of Fx (5–30 µM).The levels of α-smooth muscle actin (α-SMA), Col-1, and phosphorylated (p)-Smad 2/3, signal protein-1 (SP-1), MAPKs (mitogen-activated protein kinases), and Akt were measured by western blot analysis.

The expression of Col-1 was detected in NP tissues.TGF-β1 here stimulated the production of α-SMA and Col-1, and stimulated the contraction of collagen gel.However, pretreatment with Fx attenuated these effects.

Furthermore, these inhibitory effects were mediated through modulation of both Smad 2/3 and Akt/SP-1 signaling pathways in TGF-β1-induced NPDFs.The results from the present study suggest that Fx may be a novel anti-fibrotic agent for the treatment of NP formation.

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