Effects And Mechanism Of GLP-1 Analogues On BLM-Induced Pulmonary Fibrosis In Mice

objective: To explore the potential value of GLP-1 in the treatment of pulmonary inflammation and pulmonary fibrosis in mice,we investigated the effect of possible mechanism associated with the Pi3k/AKT pathway during the treatment.Methods: In this study,we divided mice into 5 groups randomly: normal control group(A),BLM model group(B),GLP-1 control group(C),two group of low and high concentration of liraglutide(D and E).Among these groups,B?D and E was given Intraperitoneal injection of bleomycin.To replicate the pulmonary fibrosis model,lillarutin was injected subcutaneously in group C,D and E.While groups A and B were given subcutaneous injection of the same amount of normal saline every day.At the end of 40 days,the skin color and eye color of mice were recorded.Themorphological changes and collagen deposition of lung tissue were analyzed by Masson staining.Western Blot was used to measure the expression of Pi3 k,AKT,p-AKT,FOXO3 a and other factors related to the AKT signaling pathway.Results: Compared with N and GLP-1 groups,collagen express higher in lung tissue of BLM mice,which express lower in BLM + lira0.2 and BLM + lira0.4 compared with BLM group,but its expression is higher than that in the N and GLP-1groups.Compared with the N group and GLP-1 group,the expression of p-AKT and Pi3 k in the lung tissue of mice in the BLM group are significantly increased.While in the lung tissue of BLM+ lira0.4 and BLM+ lira0.2 groups,the expression of p-AKT and Pi3 k was down-regulated compared with those in the BLM group,but the expression was still higher than those in the N group and GLP-1 group.However,the expression of FOXO3 a has showed the opposite trend.