Astragaloside IV alleviates silica-induced pulmonary fibrosis via inactivation of the TGF-β1/Smad2/3 signaling pathway

The aim of the present study was to investigate the anti-fibrotic effects of astragaloside IV (ASV) in silicosis rats, and to further explore the potential underlying molecular mechanisms. A silica-induced rat model of pulmonary fibrosis was successfully constructed. Hematoxylin and eosin and Masson's trichrome staining were performed to observe the pathological changes in lung tissues. Immunohistochemical analysis was used to assess the expression levels of Collagen I, fibronectin and α-smooth muscle actin (α-SMA). A hemocytometer and Giemsa staining were used to evaluate the cytological characteristics of the bronchoalveolar lavage fluid. ELISA was used to detect the levels of the inflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β and IL-6. Reverse transcription-quantitative PCR and western blotting were performed to detect the mRNA and protein expression levels of genes associated with the transforming growth factor (TGF)-β1/Smad signaling pathway. ASV alleviated silica-induced pulmonary fibrosis, and reduced the expression of collagen I, fibronectin and α-SMA. In addition, the results of the present study suggested that the ASV-mediated anti-pulmonary fibrosis response may involve reduction of inflammation and oxidative stress. More importantly, ASV suppressed silica-induced lung fibroblast fibrosis via the TGF-β1/Smad signaling pathway, thereby inhibiting the progression of silicosis. In conclusion, the present study indicated that ASV may prevent silicosis-induced fibrosis by reducing the expression of Collagen I, fibronectin and α-SMA, and reducing the inflammatory response and oxidative stress, and these effects may be mediated by inhibiting the activation of the TGF-β1/Smad signaling pathway.