Effects of β-Sitosterol from Corn Silk on TGF-β1-Induced Epithelial–Mesenchymal Transition in Lung Alveolar Epithelial Cells

Pulmonary fibrosis is a chronic lung disease characterized by abnormal accumulation of the extracellular matrix (ECM). Chronic damage of the alveolar epithelium leads to a process called “epithelial–mesenchymal transition” (EMT) and increases synthesis and deposition of ECM proteins. Therefore, inhibition of EMT might be a promising therapeutic approach for the treatment of pulmonary fibrosis. β-Sitosterol is one of the most abundant phytosterols in the plant kingdom and the major constituent in corn silk, which is derived from the stigma and style of maize ( Zea mays ). In this study, we elucidated that β-sitosterol inhibited transforming growth factor-β1 (TGF-β1)-induced EMT and consequently had an antifibrotic effect. β-Sitosterol (1–10 μg/mL) significantly downregulated the TGF-β1-induced fibrotic proteins, such as collagen, fibronectin, and α-smooth muscle actin in human alveolar epithelial cells ( p < 0.01). After 24 h, relative wound density (RWD) was increased in TGF-β1 treated group (82.16 ± 5.70) compare to the control group (64.63 ± 2.21), but RWD was decreased in β-sitosterol cotreated group (10 μg/mL: 71.54 ± 7.39; 20 μg/mL: 65.69 ± 6.42). In addition, the changes of the TGF-β1-induced morphological shape and protein expression of EMT markers, N -cadherin, vimentin, and E -cadherin, were significantly blocked by β-sitosterol treatment ( p < 0.01). The effects of β-sitosterol on EMT were found to be associated with the TGF-β1/Snail pathway, which is regulated by Smad and non-Smad signaling pathways. Taken together, these findings suggest that β-sitosterol can be used to attenuate pulmonary fibrosis through suppression of EMT by inhibiting the TGF-β1/Snail pathway.