OBJECTIVE: To study the effects and mechanism of Shenqihuatan formula (参七化痰方, SQHT) of the transforming growth factor-beta (TGF-β)-stimulated cell processes in airway remodeling. METHODS: The current study examined cell viability using a Cell Counting Kit-8 assay. Furthermore, a Transwell assay was conducted to detect the ability of cell migration, and apoptosis was detected via flowcytometry. Western Blot and quantitative real-time polymerase chain reaction (qRT-PCR) were used to determine the expression levels of apoptosis or inflammation-related factors, such as TGF-β, Interleukin-1β (IL-1β), B cell lymphoma 2 (Bcl-2), Bcl-2-Associated X (Bax), Ras homolog gene family, member A (RhoA), recombinant rho associated coiled coil containing protein kinase 1/2 (ROCK1/2), extracellular regulated protein kinases 1/2 (ERK1/2), Snail, and Slug. Finally, the expression levels of matrix metalloproteinase-9 (MMP-9) and Tissue inhibitor of metalloproteinase (TIMP-1) were admeasured by enzyme-linked immuno sorbent assay. RESULTS: The results demonstrated that SQHT inhibited the viability and migration, as well as the the F-actin formation and cytoskeletal reorganization of airway smooth muscle cells (ASMCs) stimulated by TGF-β. By monitoring the changes of critical regulators in the presence of the formula, it was observed that the expression levels of TGF-β, IL-1β, Bcl-2, RhoA, ROCK1/2, ERK1/2, Snail, and Slug were markedly suppressed, whereas Bax expression exhibited the opposite effect. Compared with a well-characterized RhoA pathway inhibitor, Fasudil, SQHT generated equivalent or even higher inhibitory effects on these processes in ASMCs. CONCLUSIONS: Collectively, these suggested that SQHT can reduce airway inflammation by inhibiting TGF-β-stimulated signaling pathways in ASMCs. These findings may provide a novel remedy for treating ASMC inflammation, which causes thickening and obstruction of the airway in chronic obstructive pulmonary disease.