Abstract

Abstract Polygonum cuspidatum (PC) extract has effect on silica-induced pulmonary fibrosis. This study aimed to explore the anti-pulmonary-fibrosis effects and mechanism of PC. Sprague–Dawley rat model was constructed by inhalation of silicon dioxide suspension through tracheal intubation method. And histopathological examination showed that PC inhibited inflammatory cell infiltration, fibrous and collagen hyperplasia, and protected the normal structure of alveoli. TUNEL assay declared that PC retarded cell apoptosis. Meanwhile, up-regulation of basic fibroblast growth factor, plated-derived growth factor, and TNF-α in silicosis rats was decreased by PC addition. In addition, human fetal lung fibroblasts (HFL-1) cells were stimulated with transforming growth factor-β1 (TGF-β1). PC administration increased the proliferation and invasion of TGF-β1-stimulated HFL-1 cells whereas decreased cell apoptosis. Moreover, western blotting exhibited that PC treatment decreased the expression of α-smooth muscle actin, collagen I, and collagen III in silicosis rats and TGF-β1-stimulated HFL-1 cells. Furthermore, the levels of Wnt/β-catenin pathway proteins were up-regulated in silicosis rats and TGF-β1-stimulated HFL-1 cells, which were weakened by PC treatment. Meanwhile, Wnt3a (an activator of Wnt/β-catenin) addition reversed the effect of PC addition. In conclusion, PC prevents silica-induced fibrosis through inhibiting the Wnt/β-catenin pathway.

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