Aim To investigate the role of scavenger receptor CD36 in carboxy methyl lysine (CML) inhibition of foam cell migration. Methods (1)The effect of CML on lipid accumulation and cell migration of RAW264.7 macrophages was observed, followed by observing the interaction of CML with CD36. The experiment was divided into:control group, oxidized low density lipoprotein (ox-LDL) group (40 mg/L ox-LDL), CML group (40 mg/L ox-LDL+10 μmol/L CML); (2)To observe the role of CD36 in CML inhibition of foam cell migration, the experiment was divided into two parts. Firstly, the effects of CD36 inhibitor SSO on the migration of RAW264.7 foam cells was investigated:control group (40 mg/L ox-LDL+10 μmol/L CML) and SSO group (40 mg/L ox-LDL+10 μmol/L CML+25 μmol/L SSO); And then the effect of different receptor blockade on CML inhibition of foam cell migration was observed:control group (40 mg/L ox-LDL+10 μmol/L CML), anti-CD36 group (40 mg/L ox-LDL+10 μmol/L CML+2 μmol/L anti-CD36), anti-RAGE group (40 mg/L ox-LDL+10 μmol/L CML+2 μmol/L anti-RAGE), malBSA group (40 mg/L ox-LDL+10 μmol/L CML+400 nmol/L malBSA). Some related detections were performed after 24 h of 1%BSA medium intervention (oil red O staining, Transwell cell migration experiments, immunoprecipitation experiments, CD36 immunofluorescence staining, etc). Results Cholesterol oxidase method quantification and oil red O staining qualitative showed that CML can effectively promote the accumulation of lipid droplets in RAW264.7 macrophages and form key components of atherosclerotic plaques--foam cells. Transwell cell migration experiments and quantitative analysis showed that:compared with the control group, the number of migrating foam cells in the ox-LDL group decreased by 43.5%(P<0.05); Compared with ox-LDL group, CML reduced the number of foam cell migration by 49.2%(0.287±0.031 vs 0.565±0.061,P<0.05),the result indicated that CML inhibited RAW264.7-derived foam cell migration. Immunoprecipitation experiments and immunofluorescence staining showed that there was a significant interaction between CML and CD36 in foam cells. Further more, after using SSO or neutralizing antibody anti-CD36 to block CD36 and scavenger receptor inhibitor malBSA block all scavenger receptors, the number of migrated cells was significantly higher than that of the control group(P<0.05). Statistical analysis showed that, the cell migration index of anti-CD36 group was 81.3% in malBSA group(2.35±0.39 vs 2.89±0.41, P<0.05). Conclusion Scavenger receptor CD36 may be a key node for CML inhibition of RAW264.7 foam cell migration.