Objective：To investigate the effects and potential mechanisms of liraglutide（Li）on macrophages polarization induced by silica（SiO₂）. Methods：Macrophages were divided into five groups：the control group，SiO₂ group，SiO₂+Li（10 nmol/L）group，SiO₂+Li （100 nmol/L）group，and SiO₂+Li（1 000 nmol/L）group. The cytotoxicity of Li on the macrophages was assessed using the CCK-8 assay； levels of interleukin（IL）-1β，IL-10 and transforming growth factor（TGF）-β1 in each group were measured by ELISA. Western blot was used to determine the expression levels of NOD-like receptor protein 3（NLRP3），cysteinyl aspartate specific proteinase（Caspase- 1）p20，and arginase-1（Arg-1）. Mitochondrial membrane potential in the macrophages was detected by using JC-1 fluorescent probe staining. Reactive oxygen species（ROS）levels in the macrophages from all groups were measured by using DCFH-DA probe. Results： Compared with the control group，the SiO₂ group showed significantly increased protein levels of NLRP3，Caspase-1 p20，and Arg-1，as well as elevated secretion of IL-1β，IL-10，and TGF-β1（all P ＜ 0.010）. Compared with the SiO₂ group，the SiO₂+Li（10 nmol/L），SiO₂+Li （100 nmol/L），and SiO₂+Li（1 000 nmol/L）groups showed decreased protein levels of NLRP3，Caspase-1 p20，and Arg-1，and reduced secretion of IL-1β，IL-10，and TGF-β1（all P ＜ 0.05）. The mitochondrial membrane potential in the SiO₂ group was lower than that in the Control group；however，it increased in the SiO₂+ Li（10 nmol/L），SiO₂+ Li（100 nmol/L），and SiO₂+ Li（1 000 nmol/L）groups compared to the SiO₂ group. The relative fluorescence intensity of ROS in the SiO₂ group was higher than that in the Control group，with statistically significant differences. Compared with the SiO₂ group，the relative fluorescence intensity of ROS in the SiO₂+Li（10 nmol/L）， SiO₂+Li（100 nmol/L），and SiO₂+Li（1 000 nmol/L）groups gradually decreased，with statistically significant differences. Conclusion：Li may inhibit SiO₂ -induced M2 macrophage polarization by improving SiO₂ -induced mitochondrial dysfunction，reducing ROS oxidative stress，and preventing NLRP3 inflammasome activation.