ABSTRACT
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.
Subject(s)
Adolescent , Child , Female , Humans , Male , Achievement , Attention Deficit Disorder with Hyperactivity/psychology , Attention/physiology , Analysis of Variance , Attention Deficit Disorder with Hyperactivity/diagnosis , Cohort Studies , Educational Status , Psychiatric Status Rating Scales , Sensitivity and SpecificityABSTRACT
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.
Subject(s)
Anticholesteremic Agents/therapeutic use , Cholesterol, HDL/blood , Cholesterol, LDL/blood , Heptanoic Acids/therapeutic use , Hypercholesterolemia/blood , Platelet Activation , Pyrroles/therapeutic use , Aged , Analysis of Variance , Atorvastatin , Biomarkers/analysis , Cholesterol, HDL/metabolism , Cholesterol, LDL/metabolism , Female , Flow Cytometry , Humans , Hypercholesterolemia/drug therapy , Male , Middle Aged , P-Selectin/blood , Platelet Aggregation/drug effects , Platelet Aggregation Inhibitors/metabolism , Platelet Glycoprotein GPIIb-IIIa Complex/analysis , Statistics, NonparametricABSTRACT
Surface modification is a conventional approach in biomaterials development, but most of the modification processes are intricate and time inefficient. In this study, a convenient open air plasma treatment was employed to modify the surface of poly(d,l-lactide) (PLA). Chitosan and fibroblast growth factor 1 (FGF1) were sequentially grafted with the assistance of open air plasma treatment onto the PLA nerve conduits with designed micropores and surface microgrooves. Grafting of these components was verified by electron spectroscopy for chemical analysis. The modified nerve conduits showed enhanced ability in the repair of 10-mm sciatic nerve transection defects in rats. The sequential air plasma treatment can be a convenient way to introduce biocompatible (e.g., chitosan) and bioactive components (e.g., growth factors) onto the surface of biomaterials.
