• Nannan Li, Feifei Feng, Ke Wu, Huanan Zhang, Wei Zhang, and Wei Wang.
• Department of Respiratory Medicine, The Second Hospital of Shandong University, Jinan, 250033, Shandong, PR China; Department of Respiratory Medicine, Central Hospital of Tai'an of Shandong Province, Tai'an, 271000, Shandong, PR China. Electronic address: 15153888050@163.com.
• Biomed. Pharmacother. 2019 Nov 1; 119: 109387.

PurposeTo observe the effect of astragaloside ASV (ASV) on silicosis fibroblasts, and further investigate its regulatory mechanism on TGF-β1/Smad3 signaling pathway.MethodsSilica-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.Results20 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.ConclusionASV 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.Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.

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