Objective：This study aims to investigate the effects of liraglutide（Li） on bleomycin（BLM）-induced pulmonary fibrosis in rat and the potential mechanisms underlying. Methods：SD rats were randomly divided into four groups：control group（Con），BLM group，BLM+Li group and Li group. After BLM（4 U/kg）was intratracheally administered once to induce pulmonary fibrosis，Li（0.2 mg/kg）was subcutaneously injected daily in BLM+Li and Li group while the control group was given the same volume of normal saline. On the day 28，all rats were anesthetized and the lung tissues were rapidly excised. Pulmonary injury and pulmonary fibrosis was evaluated by the hematoxylin-eosin and masson’s trichrome staining. Mast cells were detected with toluidine blue staining. The hydroxyproline content in the lung was detected by alkali hydrolysis assay. Collagen type I alpha 1，collagen type Ⅱ alpha 1，collagen type Ⅲ alpha 1，tumor necrosis factor（TNF）-α，interleukin（IL）-6，IL-1β and transforming growth factor β1（TGF-β1）mRNA were detected by real time quantitative PCR. ELISA was performed to analyze the level of TNF-α，IL-6 and IL-1β in the lung homogenates. E-cadherin and α-smooth muscle actin（α-SMA） expression were evaluated by immunofluorescence. The protein levels of E-cadherin，zona occluden 1（ZO-1），Occludin，α-SMA and TGF-β1 were detected by Western blot. Results：Compared with the BLM group，Li reduced inflammatory cell infiltration，interstitial thickness，collagen deposition，significantly reduced the expression of TNF-α，IL-6，IL-1β and TGF-β1；up-regulated the expression of E-cadherin，ZO-1，Occludin and down-regulated the expression of α-SMA. Conclusion：Li attenuates BLM-induced pulmonary fibrosis in rat，which might be attributed to its effects on alleviating inflammation，suppressing the expression of TGF-β1 and inhibiting epithelial-mesenchymal transition. Li might be a potential therapeutic option for pulmonary fibrosis in the future.