the specific compound exerting protective effects. Nevertheless, some studies measured the effects of single compounds, such as resveratrol, quercitin, or curcumin \[[@B175]\]. Irrespective of their source, one of the main effects exerted by the polyphenols is the NO-dependent vasodilatation ([Figure 4](#fig4){ref-type="fig"}). For example, in isolated arteries of rabbits, Karim et al. demonstrated that cocoa extracts increased levels of intracellular Ca^2+^, leading to L-arginine conversion in citrulline and to the eNOS activation \[[@B176]\]. Similarly, plant-derived polyphenols have been reported to induce vasodilatation of porcine coronary arteries through NO generation \[[@B177]\]. Moreover, in bovine endothelial cells, catechins of green tea activated eNOS by phosphorylation at Ser1179 and dephosphorylation at Thr495 in a PKA-Akt dependent manner \[[@B178], [@B179]\]. In addition, such compounds were also shown to exert protective effects in diabetic rats thanks to the reduction of oxidative stress obtained by downregulation of NADPH oxidase \[[@B180]\]. Interestingly, catechins were found to reduce platelet aggregation and to reverse endothelial dysfunction in patients with coronary artery disease, thus exerting antiatherosclerotic properties \[[@B181], [@B182]\]. Moreover, polyphenols of the black tea were found to enhance the activity of eNOS via p38 MAPK-dependent phosphorylation in porcine aortic endothelial cells. In fact, both pharmacological and genetic inhibition of p38 MAPK attenuated both eNOS activation and phosphorylation changes in response to these polyphenols \[[@B183]\].

Among plant-derived polyphenols, fruit extracts of*Camelia japonica*(CJF), a plant widely distributed in Asia and well known for its antioxidant properties \[[@B184]\], have been demonstrated to induce the NO production via Akt pathways in endothelial cells and to activate eNOS via phosphorylation at Ser1179. In the same study, CJF inhibited VSMCs proliferation and migration, suggesting its beneficial role in the preventio