RESUMO
High levels of low-density lipoprotein cholesterol (LDL-C) enhance platelet activation, whereas high levels of high-density lipoprotein cholesterol (HDL-C) exert a cardioprotective effect. However, the effects on platelet activation of high levels of LDL-C combined with low levels of HDL-C (HLC) have not yet been reported. We aimed to evaluate the platelet activation marker of HLC patients and investigate the antiplatelet effect of atorvastatin on this population. Forty-eight patients with high levels of LDL-C were enrolled. Among these, 23 had HLC and the other 25 had high levels of LDL-C combined with normal levels of HDL-C (HNC). A total of 35 normocholesterolemic (NOMC) volunteers were included as controls. Whole blood flow cytometry and platelet aggregation measurements were performed on all participants to detect the following platelet activation markers: CD62p (P-selectin), PAC-1 (GPIIb/IIIa), and maximal platelet aggregation (MPAG). A daily dose of 20 mg atorvastatin was administered to patients with high levels of LDL-C, and the above assessments were obtained at baseline and after 1 and 2 months of treatment. The expression of platelets CD62p and PAC-1 was increased in HNC patients compared to NOMC volunteers (P<0.01 and P<0.05). Furthermore, the surface expression of platelets CD62p and PAC-1 was greater among HLC patients than among HNC patients (P<0.01 and P<0.05). Although the expression of CD62p and PAC-1 decreased significantly after atorvastatin treatment, it remained higher in the HLC group than in the HNC group (P<0.05 and P=0.116). The reduction of HDL-C further increased platelet activation in patients with high levels of LDL-C. Platelet activation remained higher among HLC patients regardless of atorvastatin treatment.
Assuntos
Adolescente , Criança , Feminino , Humanos , Masculino , Logro , Transtorno do Deficit de Atenção com Hiperatividade/psicologia , Atenção/fisiologia , Análise de Variância , Transtorno do Deficit de Atenção com Hiperatividade/diagnóstico , Estudos de Coortes , Escolaridade , Escalas de Graduação Psiquiátrica , Sensibilidade e EspecificidadeRESUMO
High levels of low-density lipoprotein cholesterol (LDL-C) enhance platelet activation, whereas high levels of high-density lipoprotein cholesterol (HDL-C) exert a cardioprotective effect. However, the effects on platelet activation of high levels of LDL-C combined with low levels of HDL-C (HLC) have not yet been reported. We aimed to evaluate the platelet activation marker of HLC patients and investigate the antiplatelet effect of atorvastatin on this population. Forty-eight patients with high levels of LDL-C were enrolled. Among these, 23 had HLC and the other 25 had high levels of LDL-C combined with normal levels of HDL-C (HNC). A total of 35 normocholesterolemic (NOMC) volunteers were included as controls. Whole blood flow cytometry and platelet aggregation measurements were performed on all participants to detect the following platelet activation markers: CD62p (P-selectin), PAC-1 (GPIIb/IIIa), and maximal platelet aggregation (MPAG). A daily dose of 20 mg atorvastatin was administered to patients with high levels of LDL-C, and the above assessments were obtained at baseline and after 1 and 2 months of treatment. The expression of platelets CD62p and PAC-1 was increased in HNC patients compared to NOMC volunteers (P<0.01 and P<0.05). Furthermore, the surface expression of platelets CD62p and PAC-1 was greater among HLC patients than among HNC patients (P<0.01 and P<0.05). Although the expression of CD62p and PAC-1 decreased significantly after atorvastatin treatment, it remained higher in the HLC group than in the HNC group (P<0.05 and P=0.116). The reduction of HDL-C further increased platelet activation in patients with high levels of LDL-C. Platelet activation remained higher among HLC patients regardless of atorvastatin treatment.
Assuntos
Anticolesterolemiantes/uso terapêutico , HDL-Colesterol/sangue , LDL-Colesterol/sangue , Ácidos Heptanoicos/uso terapêutico , Hipercolesterolemia/sangue , Ativação Plaquetária , Pirróis/uso terapêutico , Idoso , Análise de Variância , Atorvastatina , Biomarcadores/análise , HDL-Colesterol/metabolismo , LDL-Colesterol/metabolismo , Feminino , Citometria de Fluxo , Humanos , Hipercolesterolemia/tratamento farmacológico , Masculino , Pessoa de Meia-Idade , Selectina-P/sangue , Agregação Plaquetária/efeitos dos fármacos , Inibidores da Agregação Plaquetária/metabolismo , Complexo Glicoproteico GPIIb-IIIa de Plaquetas/análise , Estatísticas não ParamétricasRESUMO
The genus Lolium is one of the most important groupings of temperate forage grasses, including about eight recognized species that are native to some temperate and subtropical regions of the northern hemisphere. We examined genetic relationships among 18 accessions representing all Lolium species using RAPD markers. Among 50 random primers that we screened, 13 gave reproducible amplification banding patterns. Each of these 13 primers generated 19-43 scorable fragments. A total of 367 RAPD fragments were detected, of which 95.9% were polymorphic across all the Lolium accessions. Dice's coefficient of dissimilarity ranged from 0.016 to 0.622, which is indicative of substantial genetic variations in these Lolium accessions. A neighbor-joining cluster analysis, with bootstrap permutation, produced an unrooted dendrogram, which grouped 18 accessions into two main clades, supporting high bootstrap values (98 and 96%). The first clade included the self-pollinated species, L. persicum, L. temulentum, L. remotum, and L. subulatum. The cross-pollinated species, i.e., L. multiflorum, L. perenne, L. rigidum, and L. canariense, composed the second clade, in which L. canariense formed a distinct subclade, indicating its higher genetic separation from other allogamous species. The value of r = 0.97 in the Mantel test for cophenetic correlation applied to the cluster analysis indicated the high degree of fit of the accessions to a group. A principal coordinate analysis, whose first three coordinates explained 72.6% of the variation, showed similar groupings as in the cluster analysis. The genetic relationships estimated by the polymorphism of RAPD markers are basically in agreement with those previously inferred with other genetic markers.