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. 2014:2014:691015.
doi: 10.1155/2014/691015. Epub 2014 Aug 7.

Epicatechin and catechin modulate endothelial activation induced by platelets of patients with peripheral artery disease

R Carnevale  1 , L Loffredo  1 , C Nocella  1 , S Bartimoccia  1 , T Bucci  1 , E De Falco  2 , M Peruzzi  2 , I Chimenti  2 , G Biondi-Zoccai  2 , P Pignatelli  1 , F Violi  1 , G Frati  3
Affiliations

Epicatechin and catechin modulate endothelial activation induced by platelets of patients with peripheral artery disease

R Carnevale et al. Oxid Med Cell Longev. 2014.

Abstract

Platelet activation contributes to the alteration of endothelial function, a critical initial step in atherogenesis through the production and release of prooxidant mediators. There is uncertainty about the precise role of polyphenols in interaction between platelets and endothelial cells (ECs). We aimed to investigate whether polyphenols are able to reduce endothelial activation induced by activated platelets. First, we compared platelet activation and flow-mediated dilation (FMD) in 10 healthy subjects (HS) and 10 patients with peripheral artery disease (PAD). Then, we evaluated the effect of epicatechin plus catechin on platelet-HUVEC interaction by measuring soluble cell adhesion molecules (CAMs), NOx production, and eNOS phosphorylation (p-eNOS) in HUVEC. Compared to HS, PAD patients had enhanced platelet activation. Conversely, PAD patients had lower FMD than HS. Supernatant of activated platelets from PAD patients induced an increase of sCAMs release and a decrease of p-eNOS and nitric oxide (NO) bioavailability compared to unstimulated HUVEC. Coincubation of HUVEC, with supernatant of PAD platelets patients, pretreated with a scalar dose of the polyphenols, resulted in a decrease of sCAMs release and in an increase of p-eNOS and NO bioavailability. This study demonstrates that epicatechin plus catechin reduces endothelial activation induced by activated platelets.

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Figures

Figure 1
Figure 1
Platelet-induced oxidative stress in PAD patients. Platelet ROS production (a), platelet H2O2 concentration (b), platelet sNOX2-dp levels (c), platelet 8-iso-PGF2α production (d), platelet NOx production (e), and FMD (f) in PAD patients (n = 10) and healthy subjects (n = 10) ( *P < 0.001).
Figure 2
Figure 2
Biomarkers of HUVEC activation. sICAM1 (a), sVCAM1 (b), and E-selectin (c) levels released by HUVEC after incubation with EGF (white bar), supernatant of activated platelets from HS (SAHS) (dark gray bars), supernatant of activated PAD patients (SAPAD) (black bar), and supernatant of activated platelets from PAD patients (SAPAD), pretreated with scalar doses of epicatechin (0.1–10 μM) plus catechin (0.1–10 μM) (mix) (light gray bars) ( *P < 0.001).
Figure 3
Figure 3
HUVEC eNOS activation and NOx production. Densitometric analysis of P-eNOS/total eNOS ratio (a) and NOx production (b) in HUVEC incubated with EGF (white bar), supernatant of activated platelets from HS (SAHS) (dark gray bars), supernatant of activated platelets from PAD patients (SAPAD) (black bar), and supernatant of activated platelets from PAD patients (SAPAD), pretreated with scalar doses of epicatechin (0.1–10 μM) plus catechin (0.1–10 μM) (mix) (light gray bars) ( *P < 0.001). A representative western blot analysis of eNOS phosphorylation (a).
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