Abstract: 　Objective　To study the mechanism of NS1619 on airway remodeling in asthmatic mice. Methods A total of 24 healthy female BALB/c mice were randomly divided into 3 groups: the control group, the oval albumin (OVA) group (the asthma group) and the NS1619 group (the intervention group), 8 mice in each group. Asthma group was induced with OVA, challenged by continuous inhalation with 5% OVA from day 19 to 23, then changed to 3 times per week from day 24 to 55. Intervention group was inhaled with NS1619 (30 μmol/L) before OVA. Control group was given with normal saline. The thickness of airway smooth muscle and the area of collagen deposition in lung tissue slices were observed by HE and Masson staining, measured by a computer assisted image analysis system. The concentration of α-smooth muscle actin (α-SMA) in cells was detected by immunohistochemistry. The expression of platelet derived grouth factor-BB, PDGF-BB (PDGF-BB) in serum was measured by immunosorbent assay. Results Compared with the asthma group, the pathologic changes of lung tissue, the thickness of airway smooth muscle and collagen deposition in the group treated with NS1619 were significantly decreased (P<0.05). Compared with the asthma group, the levels of α-SMA in cells and PDGF-BB in serum in NS1619 treated group were significantly decreased (P<0.05). Conclusions NS1619 partly inhibited airway remodeling in asthmatic mice, partially by down-regulating the expression level of α-SMA and PDGF-BB.