Antithrombotic Potential of Olive Oil Administration in Rabbits with Elevated Cholesterol

Cruz, J. P. De La; Villalobos, M.A.; Carmona, José Antonio; Martin-Romero, Mercedes; Smith-Agreda, J; Cuesta, Felipe Sánchez de la

doi:10.1016/s0049-3848(00)00321-2

Cited by 56 publications

(46 citation statements)

References 25 publications

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“…At least one study in humans also reported a reduction in thromboxane production [25]. Inhibition of cyclooxygenase activity after administration of monounsaturated and/or polyunsaturated fatty acids is well documented in several models [26][27][28][29]. This effect was responsible for the beneficial effect of VOO on the thromboxane/prostacyclin ratio, an important factor in the prevention of thrombosis.…”

Section: Discussionmentioning

confidence: 96%

Dietary Virgin Olive Oil Reduces Oxidative Stress and Cellular Damage in Rat Brain Slices Subjected to Hypoxia–Reoxygenation

Correa

Muñoz‐Marín

Arrebola³

et al. 2007

Lipids

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We investigated how virgin olive oil (VOO) affected platelet and hypoxic brain damage in rats. Rats were given VOO orally for 30 days at 0.25 or 0.5 mL kg(-1) per day (doses A and B, respectively). Platelet aggregation, thromboxane B2, 6-keto-PGF(1alpha), and nitrites + nitrates were measured, and hypoxic damage was evaluated in a hypoxia-reoxygenation assay with fresh brain slices. Oxidative stress, prostaglandin E2, nitric oxide pathway activity and lactate dehydrogenase (LDH) activity were also measured. Dose A inhibited platelet aggregation by 36% and thromboxane B2 by 19%; inhibition by dose B was 47 and 23%, respectively. Virgin olive oil inhibited the reoxygenation-induced increase in lipid peroxidation (57% in control rats vs. 2.5% (P < 0.05) in treated rats), and reduced the decrease in glutathione concentration from 67 to 24% (dose A) and 41% (dose B). Brain prostaglandin E2 after reoxygenation was 306% higher in control animals, but the increases in treated rats were only 53% (dose A) and 45% (dose B). The increases in nitric oxide production (213% in controls) and activity of the inducible isoform of nitric oxide synthase (175% in controls) were both smaller in animals given VOO (dose A 84%; dose B 12%). Lactate dehydrogenase activity was reduced by 17% (dose A) and 42% (dose B). In conclusion, VOO modified processes related to thrombogenesis and brain ischemia. It reduced oxidative stress and modulated the inducible isoform of nitric oxide synthase, diminishing platelet aggregation and protecting the brain from the effects of hypoxia-reoxygenation.

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Section: Discussionmentioning

confidence: 96%

Dietary Virgin Olive Oil Reduces Oxidative Stress and Cellular Damage in Rat Brain Slices Subjected to Hypoxia–Reoxygenation

Correa

Muñoz‐Marín

Arrebola³

et al. 2007

Lipids

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“…They favour excess weight, insulin resistance [1], increased LDL cholesterol and are atherogenic [2]. On the contrary, non essential monounsaturated fatty acids, and namely its main component oleic acid, have a beneficial effect upon cholesterol metabolism and a protective role against cardiovascular diseases [3].…”

Section: Introductionmentioning

confidence: 99%

Alteration of polyunsaturated fatty acid status and metabolism in health and disease

Zamaria¹

2004

Reprod. Nutr. Dev.

118

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-Essential polyunsaturated fatty acids (PUFA) cannot be synthesised in the body and must be ingested by food. A balanced intake of both n-6 and n-3 PUFA is essential for good health. PUFA are the basic constituents of phospholipid membranes and determine cellular membrane fluidity and modulate enzyme activities, carriers and membrane receptors. They are also precursors of active metabolites known collectively as eicosanoids (prostaglandins, prostacyclins, thromboxanes and leukotrienes) which regulate our cellular functions. Studies indicate that n-3 PUFA have anti-inflammatory, antithrombotic, antiarrhythmic actions and immuno-modulating properties. Erythrocyte fatty acid status is a reflection of dietary fat intake. It also explores PUFA metabolism and gives information about the integration of these fatty acids into cellular membranes. Thus, erythrocyte fatty acid analysis can detect PUFA insufficiencies and imbalances from the diet, but also metabolic abnormalities and lipid peroxidation. It can be helpful in the prevention and the control of chronic diseases in which PUFA alterations have been observed as coronary heart diseases, hypertension, cancer, diabetes, inflammatory and auto-immune disorders, atopic eczema, Alzheimer dementia, major depression, schizophrenia, multiple sclerosis, etc.essential fatty acids / erythrocytes / metabolism / chronic diseases

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“…Diets rich in dietary polyunsaturated FAs may lower plasma HDL-C concentrations [Shepherd et al, 1978;Chong et al, 1987], whereas oleic acid-enriched diets were shown either to have no significant consequence [Mensink and Katan, 1989] or to elevate the levels of HDL-C [De La Cruz et al, 2000;Judd et al, 2002]. The mechanisms responsible for this effect and the implications they have for reverse cholesterol transport and atherogenesis are not fully understood.…”

Section: Discussionmentioning

confidence: 99%

Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco‐2 cells

Peretti

Delvin

Sinnett

et al. 2006

J of Cellular Biochemistry

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Cholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR-BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR-BI modulation by various potential effectors administered in both apical and basolateral sides of Caco-2 cells. With differentiation, Caco-2 cells increased SR-BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR-BI protein expression. Among the n-3, n-6, and n-9 fatty acid families, only eicosapentaenoic acid was able to lower SR-BI protein expression on both sides, whereas apical alpha-linolenic acid decreased SR-BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR-BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF-alpha, IFN-gamma), Caco-2 cells exhibited differential behavior. SR-BI was downregulated by lipopolysaccharide on both sides. Finally, WY-14643 fibrate diminished SR-BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR-BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR-BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools.

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Antithrombotic Potential of Olive Oil Administration in Rabbits with Elevated Cholesterol

Cited by 56 publications

References 25 publications

Dietary Virgin Olive Oil Reduces Oxidative Stress and Cellular Damage in Rat Brain Slices Subjected to Hypoxia–Reoxygenation

Dietary Virgin Olive Oil Reduces Oxidative Stress and Cellular Damage in Rat Brain Slices Subjected to Hypoxia–Reoxygenation

Alteration of polyunsaturated fatty acid status and metabolism in health and disease

Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco‐2 cells

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