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Olea europaea Linn (Oleaceae) Fruit Pulp Exhibits Hypocholesterolemic and Hepatoprotective Effects via Regulation of Peroxisome Proliferation-Activated Receptor Alpha in High-Fat Diet-Fed Rats
Abstract
Purpose: To investigate the hypocholesterolemic and hepatoprotective effects of Olea europaea Linn. (Oleaceae) fruit pulp (OFP-EA) extract in experimental rats.
Methods: Sprague–Dawley rats were fed with a normal diet, a high-cholesterol diet or high-cholesterol diets supplemented with OFP-EA extract (100 or 300 mg/kg/day p.o.) for 28 days. Plasma lipid profile such as total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL) and low-density lipoprotein (LDL) were measured using their respective commercial kits. Gross appearance and lipid content of liver samples were also analyzed. The changes in protein expressions of key enzymes such
as hydroxymethylglutaryl-CoA reductase (HMGR), acyl-CoA:cholesterol acyltransferase (ACAT), cytochrome P450 7A1 (CYP7A1) and peroxisome proliferation-activated receptor alpha (PPAR-á) in rat livers were evaluated using Western blotting.
Results: OFP-EA-extract markedly altered the increased plasma TC, TG, LDL and decreased the HDL induced by a hypercholesterolemic diet with a dose-dependent improvement on both atherogenic index and cardiac risk factor (p < 0.01 and p < 0.001 at 100 and 300 mg/kg dose, respectively). Lipid deposition in liver was attenuated significantly in hypercholesterolemic animals supplemented with OFPEA-extract (p < 0.01 at 100 and p < 0.001 at 300 mg/kg dose, respectively). Further mechanistic studies revealed that OFP-EA extract regulated the altered expressional levels of CYP7A1 and PPAR-á in the livers of hypercholesterolemic diet-induced rats.
Conclusion: The hypocholesterolemic and hepatoprotective functions of OFP-EA-extract are probably due to the increase in fatty acids unitization in liver via the up-regulation of PPAR-á level.
Keywords: Olea europaea, cholesterol, Hypercholesterolemia, Lipid metabolism, Peroxisome proliferation-activated receptor alpha.