Abstract

The development of nutraceutical ingredients has risen as a nutritional solution for health prevention. This study evaluated the effects of Oleactiv®, an ingredient developed for the prevention of atherogenesis, in hypercholesterolemic hamsters. Oleactiv® is a polyphenol-rich ingredient obtained from artichoke, olive and grape extracts as part of fruit and vegetables commonly consumed within the Mediterranean diet. A total of 21 Golden Syrian hamsters were divided into three groups. The standard group (STD) was fed a normolipidemic diet for 12 weeks, while the control group (CTRL) and Oleactiv® goup (OLE) were fed a high-fat diet. After sacrifice, the aortic fatty streak area (AFSA), plasmatic total cholesterol (TC), high-density lipoproteins (HDL-C), non-HDL-C and triglycerides (TG), were assessed. The cholesterol efflux capacity (CEC) of hamster plasma was quantified using a radiolabeled technique in murine macrophages J774. OLE administration induced a significant reduction of AFSA (−69%, p < 0.0001). Hamsters of the OLE group showed a significant decrease of both non-HDL-C (−173 mmol/L, p < 0.05) and TG (−154 mmol/L, p < 0.05). Interestingly, OLE induced a significant increase of total CEC (+17,33%, p < 0,05). Oleactiv® supplementation prevented atheroma development and had positive effects on the lipid profile of hypercholesterolemic hamsters. The increased CEC underlines the anti-atherosclerotic mechanism at the root of the atheroma reduction observed.

Highlights

  • IntroductionCardiovascular diseases (CVDs) are one of the major causes of death in Western countries.A total of 17.5 million people die each year from CVDs, corresponding to an estimated rate of 31%of all deaths worldwide [1], and this could remain the case for at least the 15–20 years [1].Nutrients 2018, 10, 1511; doi:10.3390/nu10101511 www.mdpi.com/journal/nutrientsThe main cause of the development of CVDs, atherosclerosis, has a multifactorial, gradual, and chronic etiology that is rooted in an imbalanced homeostasis of both blood lipids and oxidative status.Such disorders are responsible for a long-standing process resulting in the accumulation of modified low-density-lipoprotein-cholesterol (LDL-C) engorged macrophages, or “foam cells”, within the intima of the arterial wall, corresponding to the first step of the atheromatous plaque formation.Various factors, such as chronic inflammation, may lead to plaque rupture until the clot of vessels and rapidly induce heart or brain ischemia [2].As lipid deposits are a crucial step in foam cell accumulation and the atherosclerotic lesion progress, it appears to be an interesting target to investigate for prevention

  • Such disorders are responsible for a long-standing process resulting in the accumulation of modified low-density-lipoprotein-cholesterol (LDL-C) engorged macrophages, or “foam cells”, within the intima of the arterial wall, corresponding to the first step of the atheromatous plaque formation

  • We evaluated the effects of Oleactiv®, a polyphenol-rich ingredient obtained from the extraction of fruit and vegetables commonly consumed within the Mediterranean diet, on atherosclerosis etiology in high-fat fed and hypercholesterolemic hamsters

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Summary

Introduction

Cardiovascular diseases (CVDs) are one of the major causes of death in Western countries.A total of 17.5 million people die each year from CVDs, corresponding to an estimated rate of 31%of all deaths worldwide [1], and this could remain the case for at least the 15–20 years [1].Nutrients 2018, 10, 1511; doi:10.3390/nu10101511 www.mdpi.com/journal/nutrientsThe main cause of the development of CVDs, atherosclerosis, has a multifactorial, gradual, and chronic etiology that is rooted in an imbalanced homeostasis of both blood lipids and oxidative status.Such disorders are responsible for a long-standing process resulting in the accumulation of modified low-density-lipoprotein-cholesterol (LDL-C) engorged macrophages, or “foam cells”, within the intima of the arterial wall, corresponding to the first step of the atheromatous plaque formation.Various factors, such as chronic inflammation, may lead to plaque rupture until the clot of vessels and rapidly induce heart or brain ischemia [2].As lipid deposits are a crucial step in foam cell accumulation and the atherosclerotic lesion progress, it appears to be an interesting target to investigate for prevention. The main cause of the development of CVDs, atherosclerosis, has a multifactorial, gradual, and chronic etiology that is rooted in an imbalanced homeostasis of both blood lipids and oxidative status Such disorders are responsible for a long-standing process resulting in the accumulation of modified low-density-lipoprotein-cholesterol (LDL-C) engorged macrophages, or “foam cells”, within the intima of the arterial wall, corresponding to the first step of the atheromatous plaque formation. The main way the organism is capable of removing the excess lipid deposits and foam cell-derived cholesterol is through reverse cholesterol transport (RCT) mediated by high-density-lipoprotein (HDL-C) This mechanism, based on the cholesterol efflux capacity (CEC), manages the clearance of cholesterol from peripheral tissues, including the arterial wall, and it has recently been established to be a relevant predictor of cardiovascular risk [3,4]. The stimulation of RCT might slow down the formation and the development of atheroma [5,6]

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