Scutellarin could relieve airway inflammation and remodeling by inhibiting the EMT event as indicated by the following findings: (a) scutellarin inhibited the TGF-β1-induced migration and EMT of 16HBE cells; (b) scutellarin alleviated the ovalbumin-induced AHR, airway remodeling, and airway inflammation in mice; (c) scutellarin inhibited the EMT process in the lung tissues of ovalbumin-challenged asthmatic mice; and (d) scutellarin inactivated the Smad2/Smad3 and MAPK pathways in vivo and in vitro. Here, TGFB1 is linked to inflammation.