〔Abstract〕 Objective To observe the effects of the tofacitinib on interstitial lung disease(ILD) by regulating the JAK-STAT signaling pathway. Methods Wistar rats were randomly divided into 4 groups: normal group, ILD group, prednisone acetate group, and tofacitinib group.Except for the normal group, the other three groups were given 3 mg/ml bleomycin solution for modeling.After 28 days of intragastric administration, the lung tissues of all rats were collected for hematoxylin-eosin staining(HE) and Western blot(WB) to detect the protein levels of JAK1 and STAT1;Enzyme-linked immunosorbent assay(ELISA) was used to detect tumor necrosis factor in rat serum(TNF)-α,interleukin(IL)-6,IL-10,IL-1β. Results HE staining of lung tissue in ILD,prednisone acetate group and tofacitinib group showed alveolar tissue thickening, alveolar wall capillary congestion, bronchial luminal epithelial cells shedding, and inflammatory cell exudation.The results of WB showed that JAK1 and STAT1 significantly increased in ILD group, and decreased in different degrees compared with ILD group, tofacitinib group and prednisone acetate group(P<0.05).The ELISA results showed that the expressions of serum TNF-α,IL-6 and IL-1β in the ILD group were significantly higher than those in the normal group(P<0.01).The expression of pine group decreased(P<0.05),and the expression of IL-10 was the opposite. Conclusion Tofacitinib reduces lung tissue damage and the inflammatory response in the treatment of ILD by inhibiting the JAK-STAT pathway and down-regulating the expression of inflammatory factors TNF-α,IL-6,IL-1β and up-regulating the anti-inflammatory factor IL-10.