Multiple sclerosis (MS) is the most common chronic disabling neurological disease in young adults. Alterations in platelet function have been observed in MS; however, the mechanism and the relevance of this blood cell disorder with regard to MS pathogenesis are not yet understood. The aim of this study was to evaluate activities of ectonucleoside thiphosphate diphosphohydrolase (NTPDase, CD39), ectonucleotide pyrophosphatase/phosphodiesterase (E-NPP), 5'-nucleotidase and adenosine deaminase (ADA) in platelets from patients with the relapsing-remitting form of MS (RRMS), as well as to analyze platelet aggregation and expression of NTPDase. The results obtained show that NTPDase, 5'-nucleotidase, E-NPP and ADA activities were decreased in platelets of RRMS patients when compared with the control group (p < 0.05). In addition, NTPDase expression in platelets was also decreased in these patients (p < 0.05); however, no differences were observed in platelet aggregation between RRMS patients and the control group. Our results suggest that the alterations in NTPDase, E-NPP, 5'-nucleotidase and ADA may have contributed to the alterations in platelet function in MS by altering the levels of nucleotides and nucleosides in the circulation.

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The effect of quercetin was assessed in rats induced with complete Freund adjuvant (CFA). Arthritis scores, paw oedema, latency, activities of myeloperoxidase (MPO), ectonucleoside triphosphate diphosphohydrolase (E‐NTPDase), and ectoadenosine deaminase (E‐ADA) in lymphocytes were determined. Furthermore, nucleotide and nucleoside levels as well as the secretion of pro‐ and anti‐inflammatory cytokines were evaluated. Animals were treated with saline and quercetin in doses of 5, 25, and 50 mg/kg for 45 days. The result revealed that quercetin (50 mg/kg) reduced arthritis score and paw oedema, and increased the latency in the thermal hyperalgesia test. Histopathological analysis showed that all the doses of quercetin reduced infiltration of inflammatory cells. MPO activity was increased in the arthritis group; however, quercetin reduced this activity. E‐NTPDase activity was increased in lymphocytes of arthritis rats, and treatment with quercetin reversed this increase. However, E‐ADA activity was reduced in the arthritis group, and treatment with quercetin modulated the activity of this enzyme in arthritis rat groups. Serum adenosine levels were increased in arthritis, and the levels were lowered with quercetin treatment. Quercetin treatment in arthritis groups decreased the elevated levels of cytokines in the arthritis control group. Thus, quercetin demonstrated an anti‐inflammatory effect, and this flavonoid may be a promising natural compound for the treatment of arthritis.Significance of the studyQuercetin may represent a potential therapeutic compound in the treatment of rheumatoid arthritis. Findings from this study indicate that quercetin suppresses swelling and attenuates the underlying inflammatory responses. This is the first report where quercetin was shown to modulate the immune response to arthritis via attenuation of the purinergic system (E‐NTPDase and E‐ADA activities) and the levels of IFN‐gamma and IL‐4. Thus, this work is relevant to basic research and may be translated into clinical practice.

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Aluminium (Al), a neurotoxic compound, has been investigated in a large number of studies both in vivo and in vitro. In this study, we investigated the effect in vivo of long-term exposure to Al on NTPDase (nucleoside triphosphate diphosphohydrolase) and 5'-nucleotidase activities in the synaptosomes (obtained from the cerebral cortex and hippocampus) and platelets of rats. Here, we investigated a possible role of platelets as peripheral markers in rats. Rats were loaded by gavage with AlCl(3) 50 mg/(kg day), 5 days per week, totalizing 60 administrations. The animals were divided into four groups: (1) control (C), (2) 50 mg/kg of citrate solution (Ci), (3) 50 mg/kg of Al plus citrate (Al+Ci) solution and (4) 50 mg/kg of Al (Al). ATP hydrolysis was increased in the synaptosomes from the cerebral cortex by 42.9% for Al+Ci and 39.39% for Al, when compared to their respective control (p<0.05). ADP hydrolysis was increased by 13.15% for both Al and Al+Ci, and AMP hydrolysis increased by 32.7% for Al and 27.25% for Al+Ci (p<0.05). In hippocampal synaptosomes, the hydrolysis of ATP, ADP and AMP, was increased by 58.5%, 28.5% and 25.92%, respectively, for Al (p<0.05) and 36.7%, 22.5% and 37.64% for Al+Ci, both when compared to their respective controls. ATP, ADP and AMP hydrolysis, in platelets, was increased by 172.3%, 188.52% and 92.1%, respectively in Al+Ci, and 317.9%, 342.8% and 177.9%, respectively, for Al, when compared to their respective controls (p<0.05). Together, these results indicate that Al increases NTPDase and 5'-nucleotidase activities, in synaptosomal fractions and platelets. Thus, we suggest that platelets could be sensitive peripheral markers of Al toxicity of the central nervous system.