Protective Effects of Polyphenols Present in Mediterranean Diet on Endothelial Dysfunction

Table 1

Outlined effects of quercetin, catechin, resveratrol, and urolithin studied in vitro, in animals, and in humans.

Molecule	Study type	Mechanisms	Refs.
Quercetin	In vitro	Reduces TNF-α-induced expression of ICAM-1; Inhibits VCAM-1 and E-selectin expression, as well as COX-2 and iNOS; Activates the expression of HIF-1α and regulates glucose and hypoxia homeostasis	[31]; [32]; [33]
	Animal	Induces reduction of fatty acid and triacylglycerol synthesis and inhibits LDL oxidation; Increases Akt phosphorylation, eNOS phosphorylation, and NO production; Increases expression of VEGF; Downregulates cytochrome p450 2b genes, steroid, and cholesterol synthesis	[26, 27]; [28, 29]; [30]; [34, 35]
	Human	Reduces cellular senescence	[25]
Catechin	In vitro	Improves redox imbalance and mitochondrial dysfunction by AMPK and ACC phosphorylation; Inhibits TNF-α-induced insulin signaling pathway and induces PGC-1α expression	[47]; [48]
	Animal	Exerts beneficial effects on aortic expression of endothelial dysfunction biomarkers (VCAM-1, ICAM-1, E-selectin, LOX-1, TNF-α, and IL-6)	[46]
	Human	Increases flow-mediated dilation, reduces pulse wave velocity and diastolic blood pressure; Increases thermogenesis, reduces adipogenesis, and promotes fat oxidation	[39–41]; [42, 43]
Resveratrol	In vitro	Reduces cholesterol peroxidation, reactive oxygen species levels, and platelet aggregation by promoting vasodilation through NO synthesis and inhibition of endothelin-1; Lowers proinflammatory mediators IL-8 and ICAM-1 in TNF-α-activated endothelial cells	[50–52]; [53]
	Animal	Ameliorates endothelial dysfunction through PPARδ and SIRT1 activation; Increases expression of AMPKα, activates fatty acid mobilization and degradation, and inhibits fatty acid synthesis	[56]; [22]
	Human	Increases branchial flow-mediated dilation response; Rises the expression of AMPK, SIRT1, and PGC-1α protein levels	[54, 55]; [59]
Urolithin	In vitro	Inhibits monocyte adhesion, endothelial cell migration, and CCL-2 and IL-8 expressions; Inhibits iNOS and decreases proinflammatory cytokines expression (IL-1β, TNF-α, and IL-6); Improves NO production and eNOS activity in a dose-dependent manner and suppresses the expression of TNF-α, IL-6, ICAM-1, MCP-1, and endothelin 1 and increases PPAR-γ mRNA levels	[61]; [63, 64]; [66]
	Animal	Reduces LDL cholesterol, triglycerides, free fatty acids, and oxidative stress; Reduces ventricular hypertrophy and arrhythmia	[67, 68]; [68]
	Human	Improves endothelial function through improvements in flow-mediated dilation	[65]