The beneficial effects of virgin olive oil against oxidative stress induced by hypercholesterolemia in rats

Cardiovascular disease(CVD) remains the major cause of mortality in the world, typically claiming a third of all deaths. The primary cause of CVD is atherosclerosis. Therefore, timely prevention and therapy of atherosclerosis are able to reduce the risk of the development of its clinical manifestations. Anti-atherosclerotic activity of medicinal plants mainly appears in their multiple effects.This study was carried out to evaluate the hypolipidemic activity of virgin olive oil in experimentally induced hyperlipemic Wistar. A total of 24 rats were randomly allocated to 4 equal groups and treated as follows for 50 days: (1) Normal control (NC); that were fed with a standart diet; (2) High Cholesterol Diet Control (HCD); which received high cholesterol diet for 50 days; (3) Animals receiving high cholesterol diet for 50 days, after this period the animals are fed for eight days by the standard foodand receiving by gavage virgin olive oil (HCD+VOO) and(4) Animals fed for eight days with the standard food and receiving by gavage olive oil (VOO). High Cholesterol Diet containing yolk egg and coconut oil. Results showed that olive oil caused a significant (p < 0.01) reduction in serum levels of Total Cholesterol (TC), Triglycerides (TG), Low­Density Lipoprotein Cholesterol (LDL) and Atherogenic Index Serum (AIS). The results also demonstrated a significant (p < 0.01) increase in High­Density Lipoprotein Cholesterol (HDL). Moreover, virgin olive oil induced a significant reduction in liver lipid content. On the other hand, a High cholesterol diet induced oxidative stress was measured by estimating reduced glutathione level and amount of thiobarbituric acid reactive substances (TBARS) formed as an index of lipid peroxidation in a liver and a heart. Virgin olive oil supplementation attenuated all these variations. Our observations of the study indicate that the virgin olive oil has a significant antihyperlipidemic potential.

Redução do marcador inflamatório TNF-α após consumo de semente de linhaça por coelhos hipercolesterolemicos / Decrease in the inflammatory marker TNF-a after comsumption of flaxseed by hypercholesterolemic rabbits

Background: Functional foods such as flaxseed have been commonly consumed to prevent atherosclerosis. Objectives: To assess the effects of flaxseed in atherogenesis in rabbits consuming a high-cholesterol diet. Methods: Thirty male albino rabbits were randomized to three groups based on a 12-week dietary treatment: control group (G1), standard diet; high-cholesterol diet (G2), standard diet plus 0.25% cholesterol from lyophilized eggs; and high-cholesterol plus flaxseed (G3), similar diet as G2 plus flaxseed. Biochemical (total cholesterol [TC], high-density lipoprotein [HDL-C], low-density lipoprotein cholesterol [LDL-C], and triglycerides) and immunohistochemical (intercellular adhesion molecule 1 [ICAM-1] and tumor necrosis factor alpha [TNF- α ]) analyses were performed in all groups. P values < 0.05 indicated statistical significance. Results: At 12 weeks, serum TC levels increased significantly in G2 and G3 compared with G1. Serum LDL-C levels were higher in group G2, and the increase in group G3 was approximately six times lower than that in G2. HDL-C levels increased in all groups, with the highest increase observed in G2. Triglycerides levels in G3 decreased by ~70% and differed significantly in G1 and G3 (p = 0.034) and G2 and G3 (p = 0.015). ICAM-1 levels increased only in aortic segment 4 in G3. TNF- α levels in G3 were similar to those in the control group, while the levels in G2 were greater than twice as those in the control group (p < 0.05). Conclusions: The group fed with a functional diet (flaxseed) showed decreased development of atherosclerosis, reduced serum triglycerides levels, and lower TNF- α levels on immunohistochemistry

Fundamentos: Alimentos funcionais, como a linhaça, têm sido consumidos com frequência para prevenção da aterosclerose. Objetivos: Avaliar os efeitos da linhaça sobre a aterogênese em coelhos submetidos a uma dieta rica em colesterol. Métodos: Trinta coelhos albinos machos foram randomizados em três grupos com base em um tratamento dietético por 12 semanas: grupo controle (G1), dieta padrão; dieta rica em colesterol (G2), dieta padrão mais 0,25% de colesterol proveniente de ovos liofilizados; e dieta rica em colesterol mais linhaça (G3), dieta semelhante à do G2 adicionada de linhaça. Análise bioquímica (colesterol total [CT], lipoproteína de alta densidade [HDL-colesterol], lipoproteína de baixa densidade [LDL-colesterol] e triglicérides) e imunohistoquímica (molécula de adesão intercelular 1 [ICAM-1] e fator de necrose tumoral alfa [TNF- α ]) foram realizadas em todos os grupos. Valores de p < 0,05 indicaram significância estatística. Resultados: Às 12 semanas, os níveis séricos de CT aumentaram significativamente nos grupos G2 e G3 em comparação com o G1. Os níveis séricos de LDL-colesterol foram mais altos no grupo G2, e o aumento no grupo G3 foi cerca de seis vezes menor do que no G2. Os níveis de HDL-colesterol aumentaram em todos os grupos, com o maior aumento observado no G2. Os níveis de triglicérides no G3 reduziram em ~70% e diferiram significativamente entre o G1 e G3 (p = 0,034) e G2 e G3 (p = 0,015). Níveis de ICAM-1 aumentaram apenas no segmento aórtico 4 no G3. Os níveis de TNF- α no grupo G3 foram semelhantes aos do grupo controle, enquanto os níveis no G2 foram maiores do que o dobro em relação aos do grupo controle (p < 0,05). Conclusões: O grupo alimentado com uma dieta funcional (linhaça) mostrou redução no desenvolvimento de aterosclerose, níveis séricos mais baixos de triglicérides e níveis mais baixos de TNF- α à imunohistoquímica

Elastin-derived peptides potentiate atherosclerosis through the immune Neu1-PI3Kγ pathway.

AIMS: Elastin is degraded during vascular ageing and its products, elastin-derived peptides (EP), are present in the human blood circulation. EP binds to the elastin receptor complex (ERC) at the cell surface, composed of elastin-binding protein (EBP), a cathepsin A and a neuraminidase 1. Some in vitro functions have clearly been attributed to this binding, but the in vivo implications for arterial diseases have never been clearly investigated. METHODS AND RESULTS: Here, we demonstrate that chronic doses of EP injected into mouse models of atherosclerosis increase atherosclerotic plaque size formation. Similar effects were observed following an injection of a VGVAPG peptide, suggesting that the ERC mediates these effects. The absence of phosphoinositide 3-kinase γ (PI3Kγ) in bone marrow-derived cells prevented EP-induced atherosclerosis development, demonstrating that PI3Kγ drive EP-induced arterial lesions. Accordingly, in vitro studies showed that PI3Kγ was required for EP-induced monocyte migration and ROS production and that this effect was dependent upon neuraminidase activity. Finally, we showed that degradation of elastic lamellae in LDLR(-/-) mice fed an atherogenic diet correlated with atherosclerotic plaque formation. At the same time, the absence of the cathepsin A-neuraminidase 1 complex in cells of the haematopoietic lineage abolished atheroma plaque size progression and decreased leucocytes infiltration, clearly demonstrating the role of this complex in atherogenesis and suggesting the involvement of endogenous EP. CONCLUSION: Altogether, this work identifies EP as an enhancer of atherogenesis and defines the Neuraminidase 1/PI3Kγ signalling pathway as a key mediator of this function in vitro and in vivo.