Efeitos da Euterpe oleracea Mart. (Açaí) na função plaquetária de indivíduos saudáveis

Abstract

Euterpe oleracea Mart. (açaizeiro) is a plant typical from Brazil, rich in polyphenols, which has vasodilator properties, prevents endothelial dysfunction and improves metabolic profile. However, its role on platelet function is not known. Platelets are essential for the maintenance of vascular hemostasis, but that may also participate in thrombus formation when hyperactivated, contributing to the pathogenesis of ischemic diseases. Thus, the objective of this study was to investigate the effects of açaí stone hydroalcoholic extract (ASE) on platelet aggregation and the molecular mechanisms involved. To accomplish this, blood from 15 healthy young men was collected, centrifuged and the isolated platelets incubated with 10, 50 or 100 μg / mL ASE (according to each experiment). Platelet aggregation was measured in platelet-rich plasma (PRP) and whole blood. In order to assess the effects of ASE on the platelet inhibitor nitric oxide (NO), we measured the activity and expression of the enzyme nitric oxide synthase (NOS), cGMP levels and aggregation in the presence of L-NMMA, a NOS inhibitor. Additionally, cAMP levels were quantified, the second messenger of platelet inhibitor prostacyclin. The effect of ASE on the phosphorylation of enzymes involved in platelet activation - Akt; and mitogen-activated protein kinases JNK and ERK - was measured by Western blotting. The effect of ASE on the activity of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) was measured. ASE inhibited collagen-induced PRP aggregation (baseline, 82.7 ± 5.6, ASE50, 54.0 ± 7.2, ASE100, 31.4 ± 4.1%, p <0.0001), ADP (baseline, 46.1 ± 7.5, ASE50, 32.1 ± 4.1, ASE100, 17.6 ± 2.6%, p <0.0001) and thrombin (baseline, 103.4 ± 4.5 , ASE 50, 77.2 ± 8.9, ASE100, 53.4 ± 7.1%, p = 0.0002), as well as in whole blood under stimulation with collagen (baseline, 28.0 ± 4.0, ASE50 , 19.6 ± 4.4, ASE100, 14.8 ± 2.5 Ω, p = 0.008). L-NMMA inhibited the action of ASE50 on PRP aggregation induced by ADP and thrombin. ASE did not affect the activity of NOS, nor the expression of eNOS (total and phosphorylated), but it did increase cGMP levels (baseline, 0.67 ± 0.19, ASE50, 1.50 ± 0.39, ASE100 , 1.64 ± 0.49 pmol / 108 cells, p = 0.020). Similarly, there was an increase in cAMP levels (baseline, 9.8 ± 1.8, ASE50, 13.9 ± 2.3, ASE100, 15.3 ± 2.6 pmol / 108 cells, p = 0.009). Phosphorylation of Akt, JNK and ERK enzymes was not altered. The activity of the antioxidant enzymes SOD (baseline, 0.042 ± 0.004, ASE100, 0.033 ± 0.003 U / mg ptn, p = 0.009) and CAT (baseline, 0.08 ± 0.03, ASE100, 0.05 ± 0.02 U / mg ptn, p = 0.049) but not GPx (baseline, 1.5 ± 0.6, ASE100, 1.4 ± 0.6 U / mg ptn, p = 0.312) was shown to be decreased. In view of these results, it is possible that ASE has the potential to be used in the prophylaxis and treatment of diseases associated with platelet hyperaggregability, although the mechanisms underlying this process need to be fully clarified.