Cocoa Flavanol Cardiovascular Effects Beyond Blood Pressure Reduction

Jumar, Agnes; Schmieder, Roland E.

doi:10.1111/jch.12715

Cited by 28 publications

(21 citation statements)

References 67 publications

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“…This performance may be due to the effects of flavonoids on blood pressure and peripheral and central blood flow [26, 27]. The beneficial effects of flavanols also include improved endothelial function, anti-inflammatory potency, inhibition of platelet activation, and increased vasodilatory capacity [28]. EPI is the most physiologically potent compound, and primarily accounts for the biological effects of flavanols [13].…”

Section: Discussionmentioning

confidence: 99%

(–)-Epicatechin Suppresses Angiotensin II-induced Cardiac Hypertrophy via the Activation of the SP1/SIRT1 Signaling Pathway

Dong

Wan

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Flavonol (–)-epicatechin (EPI) is present in high amounts in cocoa and tea products, and has been shown to exert beneficial effects on the cardiovascular system. However, the precise mechanism of EPI on cardiomyocyte hypertrophy has not yet been determined. In this study, we examined whether EPI could inhibit cardiac hypertrophy. Methods: We utilised cultured neonatal mouse cardiomyocytes and mice for immunofluorescence, immunochemistry, qRT-PCR, and western blot analyses. Results: 1µM EPI significantly inhibited 1µM angiotensin II (Ang II)-induced increase of cardiomyocyte size, as well as the mRNA and protein levels of ANP, BNP and β-MHC in vitro. The effects of EPI were accompanied with an up-regulation of SP1 and SIRT1, and were abolished by SP1 inhibition. Up-regulation of SP1 could block Ang II-induced increase in cardiomyocyte size, as well as the mRNA and protein levels of ANP, BNP and β-MHC, and increase the protein levels of SIRT1 in vitro. Moreover, 1 mg/kg body weight/day EPI significantly inhibited mouse cardiac hypertrophy induced by Ang II, which could be eliminated by SP1 inhibition in vivo. Conclusion: Our data indicated that EPI inhibited AngII-induced cardiac hypertrophy by activating the SP1/SIRT1 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

(–)-Epicatechin Suppresses Angiotensin II-induced Cardiac Hypertrophy via the Activation of the SP1/SIRT1 Signaling Pathway

Dong

Wan

Wang

et al. 2017

Cell Physiol Biochem

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“…Cocoa flavanols are also able to inhibit platelet activation, adhesion, and aggregation, mechanisms that play a central role in the development of endothelial dysfunction and atherosclerosis ( 109 ). Indeed, activated platelets secrete a number of adhesion molecules, such as P-selectin and C40 ligand, release inflammatory mediators into the local microenvironment ( 110 ), stimulate the chemotaxis of leukocytes to the site of inflammation ( 111 ), and generate ROS, reducing NO bioavailability and contributing to endothelial dysfunction and thrombosis ( 112 ).…”

Section: Putative Mechanismsmentioning

confidence: 99%

Cocoa, Blood Pressure, and Vascular Function

et al. 2017

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Cardiovascular disease (CVD) represents the most common cause of death worldwide. The consumption of natural polyphenol-rich foods, and cocoa in particular, has been related to a reduced risk of CVD, including coronary heart disease and stroke. Intervention studies strongly suggest that cocoa exerts a beneficial impact on cardiovascular health, through the reduction of blood pressure (BP), improvement of vascular function, modulation of lipid and glucose metabolism, and reduction of platelet aggregation. These potentially beneficial effects have been shown in healthy subjects as well as in patients with risk factors (arterial hypertension, diabetes, and smoking) or established CVD (coronary heart disease or heart failure). Several potential mechanisms are supposed to be responsible for the positive effect of cocoa; among them activation of nitric oxide (NO) synthase, increased bioavailability of NO as well as antioxidant, and anti-inflammatory properties. It is the aim of this review to summarize the findings of cocoa and chocolate on BP and vascular function.

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“…Therefore, interest has been directed towards other bioactive compounds found in fruit and vegetables, namely, polyphenols (Duthie et al , ) that might mediate the benefits independent of the abundant antioxidants. Epidemiological studies have also shown that polyphenols found in berries (Ellingsen et al , ; Li et al , ), chocolate (Jumar and Schmieder, ; Larsson et al , ), coffee (Grosso et al , ) and red wine (Cosmi et al , ) are associated with slower CVD progression. However, given their low bioavailability, the assumption that the observed health beneficial effects are driven by their direct antioxidant activity (chemical antagonism) seems very unlikely.…”

Section: Antioxidant Therapies In Cvdmentioning

confidence: 99%

Bioactive polyphenols and cardiovascular disease: chemical antagonists, pharmacological agents or xenobiotics that drive an adaptive response?

Goszcz

Duthie

Stewart

et al. 2017

British J Pharmacology

128

117

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Polyphenols are widely regarded to have a wide range of health-promoting qualities, including beneficial effects on cardiovascular disease. Historically, the benefits have been linked to their well-recognized powerful antioxidant activity. However, the concept that the beneficial effects are attributable to direct antioxidant activity in vivo does not pay sufficient heed to the fact that polyphenols degrade rapidly, are poorly absorbed and rapidly metabolized, resulting in very low bioavailability. This review explores alternative mechanisms by which polyphenols, or their metabolites, exert biological activity via mechanisms that can be activated by physiologically relevant concentrations. Evidence is presented to support the action of phenolic derivatives on receptors and signalling pathways to induce adaptive responses that drive changes in endogenous antioxidant, antiplatelet, vasodilatory and anti-inflammatory effects. The implications are that in vitro antioxidant measures as predictors of polyphenol protective activity in vivo hold little relevance and that closer attention needs to be paid to bioavailable metabolites to understand the mode of action of these diet-derived components. LINKED ARTICLESThis article is part of a themed section on Principles of Pharmacological Research of Nutraceuticals. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.11/issuetoc Abbreviations A549, adenocarcinomic human alveolar basal epithelial cells; CD62P, P-selectin; CSE, cigarette smoke extract; EGCG, epigallocatechin-3-gallate; eNOS, endothelial NOS; ER-α/β, oestrogen receptor-α/β; GR, glutathione reductase; GSL, glutamylcysteine ligase; GST, GSH-S-transferase; HO1, haem oxygenase 1; ICAM-1, intercellular adhesion molecule 1; IκB-α, inhibitor of κ-B α; Nrf2, nuclear factor E2-related factor 2;˙OH, hydroxyl radical; ONOO À , peroxynitrite; ox-LDL, oxidized LDL; VCAM-1, vascular cell adhesion molecule 1

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Cocoa Flavanol Cardiovascular Effects Beyond Blood Pressure Reduction

Cited by 28 publications

References 67 publications

(–)-Epicatechin Suppresses Angiotensin II-induced Cardiac Hypertrophy via the Activation of the SP1/SIRT1 Signaling Pathway

(–)-Epicatechin Suppresses Angiotensin II-induced Cardiac Hypertrophy via the Activation of the SP1/SIRT1 Signaling Pathway

Cocoa, Blood Pressure, and Vascular Function

Bioactive polyphenols and cardiovascular disease: chemical antagonists, pharmacological agents or xenobiotics that drive an adaptive response?

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