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Article Publish Status: FREE
Abstract Title:

Inhibitory effects of astragaloside IV on silica-induced pulmonary fibrosis via inactivating TGF-β1/Smad3 signaling.

Abstract Source:

Biomed Pharmacother. 2019 Sep 2 ;119:109387. Epub 2019 Sep 2. PMID: 31487583

Abstract Author(s):

Nannan Li, Feifei Feng, Ke Wu, Huanan Zhang, Wei Zhang, Wei Wang

Article Affiliation:

Nannan Li

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 detectα-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.

Study Type : In Vitro Study
Additional Links
Pharmacological Actions : Anti-Fibrotic : CK(46) : AC(29)

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