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Effects of Cornelian Cherry on Atherosclerosis and Its Risk Factors.

ABSTRACT: Functional food represents an important alternative management of atherosclerosis, its risk factors, and clinical complications. Atherosclerosis is characterized by microinflammation, formation of atheromatous lipoprotein-rich plaques, and protrombogenic status. Cornelian cherry (Cornus mas L., CC) contains polyphenols influencing all three components of atherosclerosis. Its high antioxidant potential, verified in experimental studies, exhibited a pronounced decrease of inflammatory markers. CC treatment demonstrated a favourable effect on lipid spectrum (comparable with statins), decrease of glycemia, and increase of insulin (comparable with glibenclamide). Polyphenols identified in CC exhibited both direct antiplatelet effects and reduction of platelet hyper-reactivity mediated via attenuation of oxidative stress. The first clinical trials confirmed a clinically relevant decrease of total and low-density lipoprotein cholesterol, triacylglycerols, lipoproteins, amelioration of inflammatory activity, and insulin secretion improvement after the treatment with CC polyphenolic compounds. However, the limitation of published studies is the use of undefined cultivars of CC, their experimental nature, small scale, and missing longitudinal trials. Nevertheless, biochemical properties of CC, hitherto described, predispose its products for the adjuvant management of atherosclerosis.

SUBMITTER: Lietava J

PROVIDER: S-EPMC6397968 | biostudies-other | 2019

REPOSITORIES: biostudies-other

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Effects of Cornelian Cherry on Atherosclerosis and Its Risk Factors.

Lietava Jan J Beerova Nikoleta N Klymenko Svetlana V SV Panghyova Elena E Varga Ivan I Pechanova Olga O

Oxidative medicine and cellular longevity 20190217

Functional food represents an important alternative management of atherosclerosis, its risk factors, and clinical complications. Atherosclerosis is characterized by microinflammation, formation of atheromatous lipoprotein-rich plaques, and protrombogenic status. Cornelian cherry (<i>Cornus mas L</i>., CC) contains polyphenols influencing all three components of atherosclerosis. Its high antioxidant potential, verified in experimental studies, exhibited a pronounced decrease of inflammatory marke ...[more]

PMID: 30911343

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Project description:Rationale: Epicardial adipose tissue (EAT) has been independently associated with non-calcified, high-risk coronary plaques in low-to intermediate risk subjects. Recently, a bidirectional communication was shown between EAT and diseased coronary arteries. In high-risk patients it is unknown whether quantitative measures of EAT can capture, and which molecular players are involved in this mutual interplay. Objective: In a high-risk population, we aimed to determine how the volume of EAT is linked to coronary artery disease (CAD) and to identify potential EAT-deregulated pathways in CAD patients specifically related to coronary artery calcification (CAC). Methods and Results: In a prospective cohort of 574 degenerative severe aortic stenosis patients referred to cardiac surgery, we quantified fat depots by computed tomography (CT) and performed a comparative quantitative proteomics of thoracic fat, including EAT, mediastinal (MAT) and subcutaneous (SAT) adipose tissues. We did not find an independent association of EAT volume with the severity, distribution and complexity of coronary stenosis in invasive coronary angiography. Although, EAT volume was correlated with high CAC, its cardiovascular risk factors-adjusted association was not significant. Taking as reference non-CAD matched-patients and compared to MAT and SAT, EAT proteomic signature of CAD was characterized by up-regulation of pro-calcifying annexins (Annexin A2, ANXA2), fatty acid binding transporters (FABP4) and inflammatory signaling proteins, and by down-regulation of fetuin-A and redox state regulatory enzymes. In EAT, ANXA2 regulation was positively correlated with CAC. EAT gene expression studies confirmed overexpression of ANXA2 and FABP4 in CAD, but no expression of FETUA was detected. Compared with non-CAD, fetuin-A circulating levels were higher in CAD, whereas no fetuin-A pericardial fluid differences were found. Conclusions: In this high-risk cohort, EAT presented an imbalance of pro-calcifying, pro-inflammatory and lipid transporters mediators. These local EAT-mediated regulatory mechanisms were not reflected by the CT volume of EAT alone.

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Project description:Previous reports suggested a role for iron and hepcidin in atherosclerosis. Here, we evaluated the causality of these associations from a genetic perspective via (i) a Mendelian randomization (MR) approach, (ii) study of association of atherosclerosis-related single nucleotide polymorphisms (SNPs) with iron and hepcidin, and (iii) estimation of genomic correlations between hepcidin, iron and atherosclerosis.Analyses were performed in a general population sample. Iron parameters (serum iron, serum ferritin, total iron-binding capacity and transferrin saturation), serum hepcidin and genome-wide SNP data were available for N = 1,819; non-invasive measurements of atherosclerosis (NIMA), i.e., presence of plaque, intima media thickness and ankle-brachial index (ABI), for N = 549. For the MR, we used 12 iron-related SNPs that were previously identified in a genome-wide association meta-analysis on iron status, and assessed associations of individual SNPs and quartiles of a multi-SNP score with NIMA. Quartile 4 versus quartile 1 of the multi-SNP score showed directionally consistent associations with the hypothesized direction of effect for all NIMA in women, indicating that increased body iron status is a risk factor for atherosclerosis in women. We observed no single SNP associations that fit the hypothesized directions of effect between iron and NIMA, except for rs651007, associated with decreased ferritin concentration and decreased atherosclerosis risk. Two of six NIMA-related SNPs showed association with the ratio hepcidin/ferritin, suggesting that an increased hepcidin/ferritin ratio increases atherosclerosis risk. Genomic correlations were close to zero, except for hepcidin and ferritin with ABI at rest [-0.27 (SE 0.34) and -0.22 (SE 0.35), respectively] and ABI after exercise [-0.29 (SE 0.34) and -0.30 (0.35), respectively]. The negative sign indicates an increased atherosclerosis risk with increased hepcidin and ferritin concentrations.Our results suggest a potential causal role for hepcidin and ferritin in atherosclerosis, and may indicate that iron status is causally related to atherosclerosis in women.

Dataset Information

Effects of Cornelian Cherry on Atherosclerosis and Its Risk Factors.

Publications

Effects of Cornelian Cherry on Atherosclerosis and Its Risk Factors.

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