〔Abstract〕 Objective To investigate the effects of liraglutide on glucocorticoid-induce osteoporosis rats and the possible mechanism. Methods Thirty healthy 8-week-old male SD rats were randomly divided into normal control group, dexamethasone group, and dexamethasone + liraglutide intervention group. After 12 weeks of intervention, BMD and bone microstructure were measured by Micro-CT. The kits were used to detect the content of reactive oxygen species(ROS), superoxide dismutase(SOD) and malondialdehyde(MDA) in bone tissue, Western blot was used to detect autophagy specific protein Beclin-1, Atg5, p62/SQSTM1 W and Map1-LC3-Ⅱ expression level. Results In the dexamethasone group, the bone density(BMD), trabecular bone volume ratio(BV/TV), trabecular bone volume(Tb.N), trabecular bone thickness(Tb.Th), and bone size of the distal femur Beam spacing(Tb.Sp) and trabecular bone connection density(Conn.D) were lower than those in the control group. The content of oxidative stress products ROS and MDA in bone tissue increased, the antioxidant enzyme SOD activity was reduced, and the expression levels of autophagy related proteins Beclin-1, Atg5 and Map1-LC3-Ⅱ increased, and the expression level of p62/SQSTM1 W protein decreased(allP<0.05). Bone density and bone microstructure of rats in the liraglutide intervention group were improved, ROS and MDA content in bone tissue reduced, antioxidant enzyme SOD activity was increased, and the expression levels of autophagy-related proteins Beclin-1, Atg5, and Map1-LC3-Ⅱ decreased, and the expression level of p62/SQSTM1 W protein increased(allP<0.05). Conclution Liraglutide can improve osteoporosis caused by glucocorticoids, and its mechanism may be related to adjusting autophagy and improving oxidative stress.