Taraxasterol inhibits TGF-β1-induced proliferation and migration of airway smooth muscle cells through regulating the p38/STAT3 signaling pathway

Abstract

Childhood asthma is a common chronic airway disease, and its severe form remains a challenging. Taraxasterol, a pentacyclic-triterpene isolated from Taraxacum officinale, has been shown to have anti-allergic property. However, the effects of taraxasterol on the proliferation and migration of airway smooth muscle cells (ASMCs) and the involved mechanisms remain unclear. Thus, the purpose of the present study was to investigate the functional role and potential molecular mechanism of taraxasterol in TGF-β1-induced ASMC proliferation and migration. Our results showed that taraxasterol significantly suppressed the transforming growth factor β1 (TGF-β1)-induced proliferation and migration of ASMCs. In addition, exposure of ASMCs to taraxasterol dramatically increased the expressions of contractile markers smooth muscle α-actin (α-SMA) and myocardin, whereas expressions of extracellular matrix (ECM) proteins type I collagen (Col I) and fibronectin were reduced in TGF-β1-stimulate ASMCs. Further studies revealed that taraxasterol suppressed the phosphorylation of p38 and signal transducer and activator of transcription 3 (STAT3) in TGF-β1-stimualted ASMCs. Notably, p38 MAPK agonist P79350 reversed the protective effects of taraxasterol on ASMCs. In conclusion, these findings indicated that taraxasterol inhibits TGF-β1-induced proliferation and migration of ASMCs through inactivation of p38/STAT3 signaling pathway.

Keywords:
asthma; taraxasterol; airway smooth muscle cells (ASMCs); p38/STAT3 pathway