Atherosclerosis　is　a　chronic　inflammatory　disease　arising　from　an　imbalance　in　lipid　levels　and　the　accumulation　of　cholesterol-laden　macrophages　in　the　artery　wall.　Crocin　is　an　active　ingredient　of　Crocus　sativus　L.　This　study　established　a　rat　coronary　atherosclerosis　model　induced　by　vitamin　D3　(VD3),　to　explore　the　effect　of　Crocin　on　lipid　metabolism,　macrophage　polarization　and　the　activity　of　inflammatory　proteins.　The　results　revealed　that　Crocin　decreased　blood　lipid　levels　by　decreasing　the　levels　of　endothelin　(ET),　total　cholesterol　(TC),　trigly-ceridelow　(TG)　and　low-density　lipoprotein　cholesterol　(LDL-c),　elevating　the　level　of　high-density　lipoprotein　cholesterin　(HDL-c).　Crocin　also　inhibited　lipogenesis　by　suppressing　the　expression　of　lipogenesis-related　proteins　and　elevating　lipid　catabolism-related　proteins.　Moreover,　Crocin　effectively　alleviated　inflammation　by　suppressing　the　expression　of　pro-inflammatory　cytokines　and　increasing　levels　of　anti-inflammatory　cytokines.　We　further　found　that　Crocin　promoted　macrophage　polarization　to　the　M2　phenotype　by　reducing　M1　markers　(CD40(+)　and　CD11c(+))　and　elevating　M2　markers　(CD613(+)　and　CD206(+)).　Finally,　Crocin　strongly　inhibited　the　expression　of　NF-kappa　B　p65　and　its　translocation　into　the　nucleus.　Crocin　partially　counteracted　nuclear　factor　kappa-light-chain-enhancer　of　activated　B　cells　(NF-kappa　B)　p65　expression　and　the　nuclei　accumulation　caused　by　NF-kappa　B　p65　overexpression.　Taken　together,　our　research　indicated　that　Crocin　inhibited　lipogenesis　and　alleviated　the　inflammation　in　a　VD3-induced　rat　coronary　atherosclerosis　model　by　promoting　M2　macrophage　polarization　and　maybe　by　inhibiting　NF-kappa　B　p65　nuclear　translocation.　This　study　implicates　Crocin　as　a　potential　therapeutic　strategy　for　coronary　atherosclerosis.