Abstract: OBJECTIVE To investigate the effects of loganin on macrophage polarization induced by advanced glycation end products (AGEs). METHODS Macrophage injury model was established by AGEs stimulation， and control group， model group， aminoguanidine group， low-dose of loganin（1 μmol/L）and high-dose of loganin（10 μmol/L）groups were set. All groups were stimulated by 100 mg/L AGEs for 24 h after dosing， respectively， except control group. ELISA assay was used to detect the secretion of IL-10， IL-12 and TNF-α. Flow cytometry was employed to measure the expression of CD86 and CD206. The expression of iNOS and CD206 were detected by immunofluorescence assay. Western blot was used to detect the expression of RAGE， RBP-J and IRF8. RESULTS The secretion of IL-12， TNF-α and the expression of iNOS， RAGE， RBP-J and IRF8 were upregulated (P<0.01). After incubated with loganin， the secretion of IL-12 and TNF-α were downregulated while IL-10 was upregulated. The expression of CD86， iNOS， RAGE， RPB-J and IRF8 were decreased while the CD206 was increased after incubation with loganin (P<0.05， P<0.01). CONCLUSION RAGE/RBP-J/IRF8 pathway may be inhibited by loganin and the M1-type polarization may be prevented. The pro-inflammatory cytokines including IL-12 and TNF-α are down-regulated while anti-inflammatory cytokine IL-10 is up-regulated to alleviate the inflammatory injury in kidney.