Background:　It　has　been　demonstrated　in　some　studies　that　triterpenoid　acid　extract　fromEriobotrya　japonica　leaf　is　beneficial　to　prevent　hyperlipidemia　or　insulin　resistance.　However,　the　effect　of　triterpenoid　acids　in　Eriobotrya　japonica　leaf　on　a　series　of　typical　symptoms　of　metabolic　syndrome　(MetS)　has　been　rarely　studied　systemati-cally.　Therefore,　the　present　study　aims　to　systematically　evaluate　the　effect　of　Eriobotrya　japonica　leaf　triterpenoid　acids　(ELTA)　on　MetS　and　explore　its　potential　mechanism.　Methods:　ELTA　(HPLC　purity　95.2　%)　was　prepared　and　administered　orally　(200　mg/kg)　to　C57BL/6　J　mice　fed　with　a　high-fat　diet　(HFD)　for　12　weeks.　Pioglitazone　(30　mg/kg)　was　used　as　a　positive　control　drug.　Food　intake,　body　weight,　total　lipid　in　feces,　lipid　profiles,　inflammatory　factors　in　serum,　hepatic　glutathione,　and　lipid　peroxide　were　measured.　Oral　glucose　tolerance　test　(OGTT)　and　insulin　tolerance　test　(ITT)　were　performed　to　evaluate　insulin　sensitivity.　RT-qPCR　and　molecular　docking　were　performed　to　explore　the　potential　mechanism.　Results:　ELTA　administration　reduced　body　weight　gain,　relative　liver　weight,　and　relative　visceral　adipose　weight.　The　levels　of　serum　total　cholesterol,　triglycerides,　low-density　lipoprotein　cholesterol,　hepatic　total　cholesterol,　and　hepatic　triglycerides　were　also　reduced.　ELTA　reduced　the　area　under　curve　(AUC)　of　blood　glucose　curves　in　OGTT　and　ITT.　Relative　mRNA　level　analysis　of　genes　related　to　MetS　showed　that　ELTA　can　effectively　increase　the　transcriptional　levels　of　Nrf2,　HO-1,　PPAR-gamma,　GluT2,　GK,　FXR,　while　effectively　decrease　those　of　PTP1B,　p65,　TNF-alpha,　IL-6,　SREBP,　11　beta　HSD-1.　Molecular　docking　showed　that　the　ligands　in　ELTA　can　bind　to　11　beta　HSD-1,　GK,　PPAR-gamma,　and　JNK,　the　important　targets　involved　in　MetS.　Conclusions:　ELTA　can　effectively　alleviate　visceral　central　obesity,　insulin　resistance,　dyslipidemia,　oxidative　stress,　and　inflammation　of　HFD-induced　MetS　in　C57BL/6　J　mice.　This　is　possibly　achieved　by　acting　on　11　beta　HSD-1,　GK,　PPAR-gamma,　and　JNK.