cardiovascular health


Proposed mechanism of action of red wine ingestion causing cardiovascular protection PDF Print E-mail

Arterioscler Thromb Vasc Biol. 2010 Jan 21. [Epub ahead of print]

Intake of Red Wine Increases the Number and Functional Capacity of Circulating Endothelial Progenitor Cells by Enhancing Nitric Oxide Bioavailability.

Huang PH, Chen YH, Tsai HY, Chen JS, Wu TC, Lin FY, Sata M, Chen JW, Lin SJ.

Division of Cardiology, Department of Internal Medicine, Department of Medical Research and Education, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Clinical Medicine, Institute and Department of Pharmacology, Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan; Graduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan; Department of Anesthesiology, School of Medicine, Taipei Medical University, Taipei, Taiwan; Division of Cardiovascular Surgery, National Defense Medical Center, Taipei, Taiwan; Department of Cardiovascular Medicine, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima, Japan.

OBJECTIVE: Red wine (RW) consumption has been associated with a reduction of cardiovascular events, but limited data are available on potential mediating mechanisms. This study tested the hypothesis that intake of RW may promote circulating endothelial progenitor cell (EPC) level and function through enhancement of nitric oxide bioavailability. METHODS AND RESULTS: Eighty healthy, young subjects were randomized and assigned to consume water (100 mL), RW (100 mL), beer (250 mL), or vodka (30 mL) daily for 3 weeks. Flow cytometry was used to quantify circulating EPC numbers, and in vitro assays were used to evaluate EPC functions. After RW ingestion, endothelial function determined by flow-mediated vasodilation was significantly enhanced; however, it remained unchanged after water, beer, or vodka intake. There were significantly increased numbers of circulating EPC (defined as KDR(+)CD133(+), CD34(+)CD133(+), CD34(+)KDR(+)) and EPC colony-forming units only in the RW group (all P<0.05). Only RW ingestion significantly enhanced plasma levels of nitric oxide and decreased asymmetrical dimethylarginine (both P<0.01). Incubation of EPC with RW (but not beer or ethanol) and resveratrol in vitro attenuated tumor necrosis factor-alpha-induced EPC senescence and improved tumor necrosis factor-alpha-suppressed EPC functions and tube formation. Incubation with nitric oxide donor sodium nitroprusside significantly ameliorated the inhibition of tumor necrosis factor-alpha on EPC proliferation, but incubation with endothelial nitric oxide synthase inhibitor L-NAME and PI3K inhibitor markedly attenuated the effect of RW on EPC proliferation. CONCLUSIONS: The intake of RW significantly enhanced circulating EPC levels and improved EPC functions by modifying nitric oxide bioavailability. These findings may help explain the beneficial effects of RW on the cardiovascular system. This study demonstrated that a moderate intake of RW can enhance circulating levels of EPC in healthy subjects by increasing nitric oxide availability. Direct incubation of EPC with RW and resveratrol can modify the functions of EPC, including attenuation of senescence and promotion of EPC adhesion, migration, and tube formation. These data suggest that RW ingestion may alter the biology of EPC, and these alterations may contribute to its unique cardiovascular-protective effect.

PMID: 20093623 [PubMed - as supplied by publisher]

 

 
Pro-inflammatory and pro-thrombotic dietary pattern increases the rate of coronary artery atherosclerosis PDF Print E-mail

Br J Nutr. 2010 Jan 22:1-9. [Epub ahead of print]

Food intake patterns associated with carotid artery atherosclerosis in the Insulin Resistance Atherosclerosis Study.

Liese AD, Nichols M, Hodo D, Mellen PB, Schulz M, Goff DC, D'Agostino RB.

Department of Epidemiology and Biostatistics and Center for Research in Nutrition and Health Disparities, Arnold School of Public Health, University of South Carolina, 800 Sumter Street, Columbia, SC 29208, USA.

We aimed to identify food intake patterns that operate via haemostatic and inflammatory pathways on progression of atherosclerosis among 802 middle-aged adults with baseline and 5-year follow-up ultrasound measurements of common (CCA) and internal carotid artery (ICA) intimal medial thickness (IMT). Food intake was ascertained with an FFQ. We derived food patterns using reduced rank regression (RRR) with plasminogen activator inhibitor 1 and fibrinogen as response variables. We explored the impact of various food pattern simplification approaches. We identified a food pattern characterised by higher intakes of less healthful foods (low-fibre bread and cereal, red and processed meat, cottage cheese, tomato foods, regular soft drinks and sweetened beverages) and lower intakes of more healthful foods (wine, rice and pasta, meal replacements and poultry). The pattern was positively associated with mean CCA IMT at follow-up (P = 0.0032), a 1 sd increase corresponding to an increase of 13 mum higher CCA IMT at follow-up, adjusted for demographic and cardiovascular risk factors. With increasing pattern quartile (Q), the percentage change in CCA IMT increased significantly: Q1 0.8 %; Q2 3.2 %; Q3 8.6 %; Q4 7.9 % (P = 0.0045). No clear association with ICA IMT was observed. All simplification methods yielded similar results. The present results support the contention that a pro-inflammatory and pro-thrombotic dietary pattern increases the rate of coronary artery atherosclerosis progression, independent of traditional cardiovascular risk factors. RRR is a promising and robust tool for moving beyond the previous focus on nutrients or foods into research on the health effects of broader dietary patterns.

PMID: 20092665 [PubMed - as supplied by publisher]

 

 
Adherence to the Mediterranean diet and risk of metabolic syndrome PDF Print E-mail

Nutr Metab Cardiovasc Dis. 2009 Oct;19(8):563-70. Epub 2009 Jan 26.

Adherence to the Mediterranean diet and risk of metabolic syndrome and its components.

Babio N, Bulló M, Basora J, Martínez-González MA, Fernández-Ballart J, Márquez-Sandoval F, Molina C, Salas-Salvadó J; Nureta-PREDIMED Investigators.  Collaborators: García-Roselló J, Isach-Subirana A, Tort VR, Marti E, Castro-Guardiola P, Mas ER, González-Pérez R, Martín-Lujan F, Sagarra AR, Cabré VJ. Human Nutrition Unit, Department of Biochemistry and Biotechnology, Faculty of Medicine and Health Sciences, Rovira i Virgili University, Spain.

BACKGROUND AND AIMS: The role of diet in the aetiology of metabolic syndrome (MetS) is not well understood. The aim of the present study was to evaluate the relationship between adherence to the Mediterranean diet (MedDiet) and MetS. METHODS AND RESULTS: A cross-sectional study was conducted with 808 high cardiovascular risk participants of the Reus PREDIMED Centre. MetS was defined by the updated National Cholesterol and Education Program Adult Treatment Panel III criteria. An inverse association between quartiles of adherence to the MedDiet (14-point score) and the prevalence of MetS (P for trend<0.001) was observed. After adjusting for age, sex, total energy intake, smoking status and physical activity, participants with the highest score of adherence to the MedDiet (>/=9 points) had the lowest odds ratio of having MetS (OR [95% CI] of 0.44 [0.27-0.70]) compared to those in the lowest quartile. Participants with the highest MedDiet adherence had 47 and 54% lower odds of having low HDL-c and hypertriglyceridemia MetS criteria, respectively, than those in the lowest quartile. Some components of the MedDiet, such as olive oil, legumes and red wine were associated with lower prevalence of MetS. CONCLUSION: Higher adherence to a Mediterranean diet is associated with a significantly lower odds ratio of having MetS in a population with a high risk of cardiovascular disease.

PMID: 19176282 [PubMed - indexed for MEDLINE]

 
Cardioprotection by resveratrol PDF Print E-mail

Cardiovasc Res. 2009 Dec 3. [Epub ahead of print]

Cardioprotection by resveratrol: A novel mechanism via autophagy involving the mTORC2 pathway.

Gurusamy N, Lekli I, Mukherjee S, Ray D, Ahsan MK, Gherghiceanu M, Popescu LM, Das DK. Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT, USA.

AIMS: Based on our previous reports that cardioprotection induced by ischemic preconditioning induces autophagy and that resveratrol, a polyphenolic antioxidant present in grapes and red wine induces preconditioning-like effects, we sought to determine if resveratrol could induce autophagy. Methods and Results Resveratrol at lower doses (0.1 and 1 microM in H9c2 cardiac myoblast cells, and 2.5 mg/kg/day in rats) induced cardiac autophagy shown by enhanced formation of autophagosomes and its component LC3-II after hypoxia-reoxygenation or ischemia-reperfusion. The autophagy was attenuated with the higher dose of resveratrol. The induction of autophagy was correlated with enhanced cell survival and decreased apoptosis. Treatment with rapamycin (100 nM), a known inducer of autophagy did not further increase autophagy compared to resveratrol alone. Autophagic inhibitors, Wortmannin (2 microM) and 3-methyladenine (10 mM), significantly attenuated the resveratrol-induced autophagy and induced cell death. The activation of mammalian target of rapamycin (mTOR) was differentially regulated by low-dose resveratrol; i.e. the phosphorylation of mTOR at serine 2448 was inhibited while the phosphorylation of mTOR at serine 2481 was increased, which was attenuated with a higher dose of resveratrol. Although resveratrol attenuated the activation of mTOR complex1, low-dose resveratrol significantly induced the expression of Rictor, a component of mTOR complex 2, and activated its downstream survival kinase Akt (Ser473). Resveratrol-induced Rictor was found to bind with mTOR. Furthermore, treatment with Rictor siRNA attenuated the resveratrol-induced autophagy. CONCLUSIONS: Our results indicate that at lower dose, resveratrol-mediated cell survival is, in part, mediated through the induction of autophagy involving mTOR-Rictor survival pathway.

PMID: 19959541 [PubMed - as supplied by publisher]

 

 

 
Dietary polyphenols PDF Print E-mail

Br J Nutr. 2009 Dec 21:1-6. [Epub ahead of print]

Physiological concentrations of dietary polyphenols regulate vascular endothelial cell expression of genes important in cardiovascular health.

Nicholson SK, Tucker GA, Brameld JM. Division of Nutritional Sciences, School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough, Leics LE12 5RD, UK.

Previous cell culture-based studies have shown potential health beneficial effects on gene expression of dietary polyphenols, including those found in red wine and green tea. However, these studies have tended to use higher concentrations (2-100 mum) than those observed in blood (0.1-1 mum) after consuming polyphenol-rich foods or beverages. The present study investigated effects of physiological concentrations of different classes of dietary polyphenol on the expression of genes important in cardiovascular health (endothelial NO synthase (eNOS), endothelin-1 (ET-1) and vascular endothelial growth factor (VEGF)) by cultured vascular endothelial cells (human umbilical vein endothelial cells) in the absence or presence of H2O2. Resveratrol and quercetin (0.1-1 mum) increased eNOS and VEGF mRNA expression particularly in the absence of H2O2 (50 mum) and decreased H2O2-induced ET-1 mRNA expression (P < 0.001 for polyphenol x H2O2 interactions). Similarly, resveratrol and quercetin decreased endothelin secretion into the media, blocking the stimulatory effect of 50 mum-H2O2 (P < 0.001 for polyphenol x H2O2 interaction). Of the nine other polyphenols tested, only epigallocatechin gallate had similar effects on both the eNOS and ET-1 mRNA expression, but to a lesser extent than resveratrol at an equimolar concentration (0.1 mum). The observed effects on gene expression would be expected to result in vasodilation and thereby reduced blood pressure. Since only three of the eleven polyphenols tested had biological activity, it is unclear whether particular structures are important or whether the effects might relate to the relatively high antioxidant capacities of the three active polyphenols.

PMID: 20021702 [PubMed - as supplied by publisher]

 


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