【Objective】To investigate the effects of zinc on the formation of atherosclerotic macrophage foaming and plaque formation and its mechanism.【Methods】The macrophage foaming model was established by stimulating THP-1 cells with oxLDL. The degree of foaming in different zinc concentrations of 0，30 and 60 μmol/Lwas detected by oil red O staining and the intake of lipid by foam cells was measured by DiI-oxLDL fluorescence. The relevant scavenger protein expression of CD36，SR-A was detected by immunoblotting. The relative expression level of zinc ion transporters was detected by real- time fluorescent quantitative PCR. ApoE-/- mice were randomly divided into 4 groups，the normal feed group（Chow group），the high- fat zinc- deficient group（HFD-ZnD），and the high- fat normal zinc group（HFD），high- fat and zinc- supplement group（HFD- ZnS），blood lipids and the protein of the mice aorta were detected in the 13 week.【Results】Compared with the normal zinc group，the oil red O density increased（P < 0.05），and add zinc ion decreased the intake of the DiI-oxLDL by foam cells（P < 0.01）. In the 0 μmol/L zinc group，the SR-A and CD36 protein expression in the foam cells increased（P < 0.05）and 15μmol/L Zn2 + treatment before stimulating with oxLDL reduced the contents of SR-A and CD36 proteins（P < 0.05）. Compared the oxLDL-treated group with the control group，the mRNA expression levels of ZIP10，ZIP12 and ZIP14 increased，and the mRNA expression levels of ZIP4，ZIP7 and ZIP8 decreased （P < 0.05）；while the mRNA expression of ZnT4 was up-regulated（P < 0.01），and the mRNA expression of ZnT1 was down- regulated（P < 0.05）. Compared with Chow group，low density lipoprotein cholesterol（LDL- C），total cholesterol（TC）and triglyceride（TG）were increased in HFD group and HFD- ZnD group，respectively（P < 0.05）；HFD- ZnD group High-density lipoprotein cholesterol（HDL-C）was significantly elevated. Moreover ，the LDL-C of the HFD-ZnS group was significantly lower than that of the HFD-ZnD group（P < 0.05）. The SR-A protein of the mice aorta of the HFD and HFD-ZnD group increased compared to the Chow group（P < 0.01），HFD-ZnS could restrain the increase（P < 0.05）. Compared with the Chow group，the ratio of plaque area in the aorta to the total arterial lumen area was significantly increased in the HFD-ZnD group（P < 0.01），and HFD-ZnS significantly inhibited this increase（P < 0.01）.【Conclusions】 Extracellular zinc deficiency aggravates lipid deposition in macrophages ，and the mechanism may be regulated by up-regulating the scavenger receptor CD36 and SR-A. Zinc ion transporters are involved in macrophage foaming and formation of arterial plaques. Zinc deficiency can increase LDL-C and promote the increase of arterial plaque induced by high-fat diet.