Alcoholic　liver　injury　is　mainly　caused　by　excessive　alcohol　consumption　and　has　become　a　global　public　health　problem　threatening　human　health.　It　is　well　known　that　Ganoderma　lucidum　possesses　various　excellent　bene-ficial　effects　on　liver　function　and　lipid　metabolism.　The　purpose　of　this　study　was　to　evaluate　the　underlying　protective　effect　and　action　mechanism　of　ganoderic　acids-rich　G.　lucidum　ethanol　extract　(GLE)　on　alcohol-induced　liver　injury　in　mice　with　excessive　alcohol　intake.　Results　showed　that　oral　administration　of　GLE　could　obviously　inhibit　the　abnormal　increases　of　serum　triglyceride　(TG),　total　cholesterol　(TC),　low　density　lipoprotein　cholesterol　(LDL-C),　aspartate　aminotransferase　(AST)　and　alanine　aminotransferase　(ALT),　and　also　significantly　protect　the　liver　against　alcohol-induced　excessive　hepatic　lipid　accumulation　and　pathological　changes.　In　addition,　alcohol-induced　oxidative　stress　in　liver　was　significantly　ameliorated　by　the　dietary　intervention　of　GLE　through　reducing　the　hepatic　levels　of　maleic　dialdehyde　(MDA)　and　lactate　dehydrogenase　(LDH),　and　increasing　the　hepatic　levels　of　glutathione　(GSH),　catalase　(CAT),　superoxide　dismutase　(SOD)　and　alcohol　dehydrogenase　(ADH).　Compared　with　the　model　group,　GLE　intervention　significantly　ameliorated　the　intestinal　microbial　disorder　by　elevating　the　relative　abundance　of　Ruminiclostridium_9,　Prevotellaceae_UCG-001,　Oscillibacter,　[Eubacterium]_xylanophilum_group,　norank_f_Clostridiates_vadinBB60_group,　GCA-900066225,　Bilophila,　Ruminococcaceae_UCG-009,　norank_f_Desulfovibrionaceae　and　Hydrogenoanaerobacterium,　but　decreasing　the　proportion　of　Clostridium_sensu_stricto_1.　Furthermore,　liver　metabolomic　profiling　suggested　that　GLE　intervention　had　a　significant　regulatory　effect　on　the　composition　of　liver　metabolites　in　mice　with　excessive　alcohol　intake,　especially　the　levels　of　some　biomarkers　involved　in　primary　bile　acid　biosynthesis,　riboflavin　metabolism,　tryptophan　metabolism,　biosynthesis　of　unsaturated　fatty　acids,　fructose　and　mannose　metabolism,　glycolysis/gluconeogenesis.　Additionally,　dietary　supplementation　with　GLE　significantly　regulated　the　mRNA　levels　of　key　genes　related　to　fatty　acids　metabolism,　ethanol　catabolism　and　inflammatory　response　in　liver.　Conclusively,　these　findings　indicate　that　GLE　has　a　potentially　beneficial　effect　on　alleviating　alcohol-induced　liver　injury　and　may　be　developed　as　a　promising　functional　food　ingredient.