Platelets and atherogenesis: Platelet anti-aggregation activity and endothelial protection from tomatoes (Solanum lycopersicum L.)

Abstract

In recent years, it has been shown that platelets are not only involved in the arterial thrombotic process, but also that they play an active role in the inflammatory process of atherogenesis from the beginning. The interaction between platelets and endothelial cells occurs in two manners: activated platelets unite with intact endothelial cells, or platelets in resting adhere to activated endothelium. In this context, inhibition of the platelet function (adhesion/aggregation) could contribute to the prevention of atherothrombosis, the leading cause of cardiovascular morbidity. This can be achieved with antiplatelet agents. However, at the public health level, the level of primary prevention, a healthy diet has also been shown to exert beneficial effects. Among those elements of a healthy diet, the consumption of tomatoes (Solanum lycopersicum L.) stands out for its effect on platelet anti-aggregation activity and endothelial protection, which may be beneficial for cardiovascular health. This article briefly discusses the involvement of platelets in atherogenesis and the possible mechanisms of action provided by tomatoes for platelet anti-aggregation activity and endothelial protection.

Figure 1.

Platelet anti-aggregation activity. Schematic diagram showing possible mechanisms of action of bioactive compounds from the tomato in inhibiting platelet aggregation. ADP, adenosine 5′-diphosphate; AC, adenilate cyclase; ATP, adenosine 5′-triphosphate; cAMP, adenosine 3′5′cyclic monophosphate; DAG, dyacil glycerole; FvW, von Willebrand Factor; GP, glycoprotein; Gq and Gi, G protein-coupled receptors; IP3, inositol 1,4,5-trisphosphate; PLCβ, phospholipase Cβ; PLCy2, phospholipase Cy2; PIP2, phosphatidylinositol 4, 5-bisphosphate; PKC, protein kinase C; PI3K, phosphoinositide 3-kinase; PKB/ Akt, protein kinase B; P2Y1 and P2Y12, ADP receptors; Rap1, ras-related protein 1; VASP, vasodilator-stimulated phosphoprotein; pVASP, phosphorylatedvasodilator-stimulated phosphoprotein.

Figure 2.

Endothelial protective mechanism. Schematic diagram showing possible mechanisms of action of bioactive compounds from the tomato in protecting endothelium. AA, arachidonic acid; AP-1, activator protein-1; BH4, tetrahydrobiopterin; COX2, cyclooxygenase 2; CRF, cardiovascular risk factor; ECE, endothelin-converting enzyme; eNOS, endothelial nitric oxide synthase; ET-1, endothelin-1; FAD, flavin adenine dinucleotide; FMN, flavin mononucleotide; ICAM-1, intercellular adhesion molecule 1; IkBα, inhibitor of I-κ-B-α; JNK, c-Jun N-terminal kinase; ox-LDL, oxidized low-density lipoprotein; MLCK/ MLC, myosin light chain kinase-myosin light chain; NADPH, nicotinamide adenine dinucleotide phosphate; NFAT, nuclear factor of activated T-cells; NFkB, nuclear factor κB; NO, nitric oxide; GP, G protein; PGI2, prostacyclin I2; PI3K, phosphoinositide 3-kinase; PLCy, phospholipase Cy; PKB/Akt, protein kinase B; p38MAPK, p38 mitogen-activated protein kinase; ROS, reactive oxygen species; TNFR1, tumor necrosis factor receptor-1; VCAM-1, vascular cell adhesion molecule-1; VEGFR1, vascular endothelial growth factor receptor-1.