Objective:To investigate the anti-hyperlipidemic effects of apple polyphenols extract(APE)in Triton WR-1339-induced endogenous hyperlipidemic model.Methods:Firstly,APE was isolated and purified from the pomace of Red Fuji Apple and contents of individual polyphenols in APE were determined using highperformance liquid chromatography-mass spectrometry(HPLC-MS).Secondly,forty male National Institude of Health(NIH)mice were randomly divided into 5 groups with 8 animals in each group.The Fenofibrate Capsules(FC)group and APE groups received oral administration of respective drugs for 7 consecutive days.All mice except those in the normal group were intravenously injected through tail vein with Triton WR-1339 on the6th day.Serum and livers from all the mice were obtained 18 h after the injection.The changes in serum total cholesterol(TC),triglyceride(TG),lipoprotein lipase(LPL)and hepatic triglyceride lipase(HTGL)were measured by respective kits.Finally,expression of hepatic peroxisome proliferator-activated receptor alpha(PPARα)mRNA was measured by real-time reverse transcription-polymerase chain reaction(RT-PCR)method.Results:Serum TC and TG levels significantly increased in Triton WR-1339-induced model group compared with the normal group(P<0.01).Oral administration of APE[200 and 400 mg/(kg·day)]dose-dependently reduced the serum level of TG in hyperlipidemic mice(P<0.01).Serum LPL and HTGL activities significantly decreased in Triton WR-1339-induced model group compared with the normal group(P<0.05).Oral administration of APE[200 and 400 mg/(kg·day)]dose-dependently elevated the serum activity of LPL in hyperlipidemic mice(P<0.05or P<0.01).Furthermore,compared with the normal group,hepatic mRNA level of PPARαin the model group significantly decreased(P<0.01).Oral administration of APE[200 and 400 mg/(kg·day)]dose-dependently elevated the expression of PPARαin hyperlipidemic mice(P<0.05 or P<0.01).Conclusion:APE could reduce TG level via up-regulation of LPL activity,which provides new evidence to elucidate the anti-hyperlipidemic effects of APE. Objective: To investigate the anti-hyperlipidemic effects of apple polyphenols extract (APE) in Triton WR-1339-induced endogenous hyperlipidemic model. Methods: Firstly, APE was isolated and purified from the pomace of Red Fuji Apple and contents of individual polyphenols in APE were determined using highperformance liquid chromatography-mass spectrometry (HPLC-MS) .Secondly, forty male National Institude of Health (NIH) mice were randomly divided into 5 groups with 8 animals in each group. The Fenofibrate Capsules (FC) group and APE groups received oral administration of respective drugs for 7 consecutive days. All mice except those in the normal group were intravenously injected through the tail vein with Triton WR-1339 on the 6th day. Serum and livers from all the mice were obtained 18 h after the injection. changes in serum total cholesterol (TC), triglyceride (TG), lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) were measured by respective kits. Finaally, expression of hepatic peroxisome proli ferator-activated receptor alpha (PPARα) mRNA was measured by real-time reverse transcription-polymerase chain reaction (RT-PCR) method. Results: Serum TC and TG levels significantly increased in Triton WR-1339-induced model group compared with the normal Oral administration of APE [200 and 400 mg / (kg · day)] dose-dependently reduced the serum level of TG in hyperlipidemic mice (P <0.01) .Serum LPL and HTGL activities significantly decreased in Triton Oral administration of APE [200 and 400 mg / (kg · day)] dose-dependently elevated the serum activity of LPL in hyperlipidemic mice (P & lt; 0.05 or P <0.01) .Furthermore, compared with the normal group, hepatic mRNA level of PPARαin the model group significantly decreased (P <0.01) .Oral administration of APE [200 and 400 mg / (kg · day)] dose- dependently elevated The expression of PPARαin hyperlipidemic mice (P <0.05 or P <0.01) .Conclusion: APE could reduce TG level via up-regulation of LPL act ivity,which provides new evidence to elucidate the anti-hyperlipidemic effects of APE.