Nanoparticles (prepared from a mixture of polyester and a polycationic polymer) loaded with insulin were prepared by a double emulsion method followed by evaporation solvent. Low molecular weight heparin (LMWH) was bound by electrostatic interactions onto the surface of the particles to confer Stealth properties. These nanoparticles were characterized in vitro (mean diameter, zeta potential, encapsulation efficiency, and release kinetics) and compared with conventional (without LMWH) and unloaded nanoparticles. The pharmacokinetics of insulin were studied after intravenous injection into diabetic rats in the form of Stealth or conventional nanoparticles or as a solution. Stealth nanoparticles allowed an increase in the elimination half-life of insulin, showing that the hydrophilic layer of LMWH was able to limit recognition by the mononuclear phagocytosis system in vivo. However, complement activation studies (CH50) did not reveal significant difference between Stealth and conventional nanoparticles.
Propranolol-HCI incorporated nanoparticles prepared with a blend of a polyester and a polycationic polymer and coated or not with a low molecular weight heparin by electrostatic interactions were prepared by emulsification followed by solvent evaporation. The mean diameter was 388 and 357 nm for coated and uncoated nanoparticles, respectively, and the entrapment efficiency ranged from 20 to 32%. Coated nanoparticles were negatively-charged, whereas uncoated nanoparticles displayed a positive zeta potential (+30 mV). After intravenous administration to rabbits of propranolol-HCI solution and propranolol-loaded nanoparticles coated or not with heparin, pharmacokinetic data revealed that coated nanoparticles exhibited a prolonged blood residence time. It can be concluded that the hydrophilic layer of heparin at the surface of nanoparticles conferred stealth properties which probably reduce the phagocytosis process and avoid immediate uptake by the mononuclear phagocytic system.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by multisystemic involvement and diverse manifestations. Neuropsychiatric systemic lupus erythematosus (NPSLE) is a complex neurological disorder characterized by neuropsychological dysfunction. NPSLE is associated with increased morbidity and mortality. In 1999, the American College of Rheumatology developed 19 discrete neuropsychiatric syndromes that comprised NPSLE. Nervous system disease in systemic lupus erythematosus is manifested by a wide variety of clinical manifestations. The pathogenesis of NPSLE is due to autoantibodies, neuronal and non neuronal antigens and the generation of proinflammatory cytokines and mediators. Anatomopathological lesions are attributed to in situ thrombosis, edema, hemorrhage, vasculitis, atherosclerosis or atheroembolism. The diagnosis of NPSLE remains largely one of exclusion and is approached by clinical evaluation, and supported when necessary by autoantibody profiles, diagnostic imaging, electrophysiologic studies and objective assessment of cognitive performance. Brain MRI abnormalities in NPSLE might show small punctate focal lesions in white matter being the most common MRI finding, followed by cortical atrophy, ventricular dilation, cerebral edema, diffuse white matter abnormalities, focal atrophy, cerebral infarction, acute leukoencephalopathy and intracranial hemorrhage. The treatment is based on the use of symptomatic therapies, immunosuppressives and non-pharmacologic interventions. This review paper was designed to understand the pathophysiology for better management of NPSLE.
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