Objective To explore the possible mechanism of Baofei Dingchuan Decoction（ 保肺定喘汤） in treating chronic obstructive pulmonary diseases（ COPD）. Methods Fifty rats were randomized into normal group

model group

herb group

western medicine group and integration group

with 10 in each group. Except the normal group

rats in other groups were made COPD models by lipopolysaccharide airway instillation combined with cigarette smoking exposure. Since the 29 th day to the 70 th day of modeling

the herb group was given Baofei Dingchuan Decoction 12. 4 g/（ kg·d） by gavage

the western medicine group was given budesonide suspension 50 μg/（ kg·d） by atomizing inhalation. The integration group was given Baofei Dingchuan Decoction by gavage and budesonide suspension by atomizing inhalation. The normal group and the model group were given normal saline 4 ml（ kg ·d） by gavage.After intervention

rats’ pulmonary arterioles were made Masson staining in each group. The changes of collagen fiber within the vascular wall and the expression ofα-smooth muscle actin（ α-SMA） were detected. Serum interleukin 6（ IL-6） level

as well as the expressions of rats’ pulmonary artery phosphorylated Janus Kinase 2（ p-JAK2） and phosphorylated signal transducersand activators of transcription 1（ p-STAT1） were detected. Results Compared with the normal group

rats’ pulmonary arterioles collagen fiber percentage and α-SMA positive cell expression in the model group decreased

with serum IL-6 level increasing and the expressions of pulmonary artery p-JAK2 and p-STAT1 increasing（ P < 0. 05 or P < 0. 01）. Compared with the model group

pulmonary arterioles collagen fiber percentage

α-SMA positive cell expression

serum IL-6 level and the expressions of pulmonary artery p-JAK2 and p-STAT1 in the Western medicine group

the herb group and the integration group decreased（ P < 0. 05 or P < 0. 01）. The expression of p-JAK2 in the integration group was lower than that in the herb group（ P < 0. 05）. Conclusion Baofei Dingchuan Decoction might reduce the vascular remodeling of COPD rats; the mechanism might relate to inhibiting JAK/STAT signaling pathways and regulating rats’ pulmonary arterioles collagen fiber andα-SMA expression.