Inhibitory effects of astragaloside IV on silica-induced pulmonary fibrosis via inactivating TGF-β1/Smad3 signaling - 01/10/19
, Feifei Feng a , Ke Wu c , Huanan Zhang a , Wei Zhang b , Wei Wang a, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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Abstract |
Purpose |
To observe the effect of astragaloside ASV (ASV) on silicosis fibroblasts, and further investigate its regulatory mechanism on TGF-β1/Smad3 signaling pathway.
Methods |
Silica-induced rats model was established in this study. RT-qPCR was performed to detect α-SMA, Collagen I, Collagen III, Smad2, Smad3 and Smad7 expression. Immunofluorescence was conducted to detect α-SMA, Collagen I, Collagen III and p-Smad3 protein and the nucleoplasmic distribution of p-Smad3.Western-blotting was performed to detect the protein of Smad2, p-Smad2, Smad3, p-Smad3 and Smad7.
Results |
20 μg/mL ASV could effectively reduce the expression of α-SMA, Collagen I, Collagen III. TGF-β1 stimulated the proliferation of fibroblasts, promoted phosphorylation of Smad2 and Smad3, and down-regulated Smad7 expression. Among them, continuous phosphorylation of Smad3 is a major factor in causing fibrosis. Besides, ASV can inhibit silica-induced lung fibroblast fibrosis through TGF-β1/Smad3 signaling pathway, thereby inhibiting the formation of silicosis.
Conclusion |
ASV could inhibit the expression of collagen in fibroblasts and the transformation to myofibroblasts, and has an anti-silicosis fibrosis effect, which may be related to the continuous phosphorylation of Smad3 in the TGF-β1/Smad signaling pathway.
Le texte complet de cet article est disponible en PDF.Abbreviations : ASV, ECM, TGF-β1, α-SMA, TβRI, TβRII
Keywords : Astragaloside ASV, Silicosis, Pulmonary fibrosis, Transforming growth factor-beta 1, Extracellular matrix
Plan
Vol 119
Article 109387- novembre 2019 Retour au numéro
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