Furthermore, we examined the anti-fibrotic effect and mechanism of SAB, and demonstrated for the first time that SAB alleviated experimental pulmonary fibrosis both in an in vivo mouse model of the disorder and in vitro. Finally, we found that the anti-pulmonary fibrotic activity of SAB was mediated by inhibition of Smad-dependent and -independent TGF-β signaling pathways. This evidence concerns the gene TGFB1 and pulmonary fibrosis.