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J Physiol Biochem ; 75(1): 89-99, 2019 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-30759305

RESUMEN

Multiple sclerosis is among the most common causes of neurological disabilities in young adults. Over the past decade, several therapeutic strategies have emerged as having potential neuroprotective and neuroregenerative properties. We investigated the effect of intranasal administration of LINGO-1-directed siRNA-loaded chitosan nanoparticles on demyelination and remyelination processes in a rat model of demyelination. Adult male Wistar rats were randomly assigned to one of 6 groups (n = 10 each) and subjected to intrapontine stereotaxic injection of ethidium bromide (EB) to induce demyelination. EB-treated rats were either left untreated or received intranasal LINGO-1-directed siRNA-chitosan nanoparticles from day 1 to day 7 (demyelination group) or from day 7 to day 21 (remyelination group) after EB injection. Chitosan nanoparticle (50 µl) was given alone after EB stereotaxic injection for both demyelination and remyelination groups. Two additional groups received 10 µl of saline by stereotaxic injection, followed by intranasal saline as controls for demyelination and remyelination groups (n = 10/group). Behavioural testing was conducted for all rats, as well as terminal biochemical assays and pathological examination of pontine tissues were done. After EB injection, rats had compromised motor performance and coordination. Pathological evidence of demyelination was observed in pontine tissue and higher levels of caspase-3 activity were detected compared to control rats. With LINGO-1-directed siRNA-chitosan nanoparticle treatment, animals performed better than controls. Remyelination-treated group showed better motor performance than demyelination group. LINGO-1 downregulation was associated with signs of repair in histopathological sections, higher expression of pontine myelin basic protein (MBP) mRNA and protein and lower levels of caspase-3 activity indicating neuroprotection and remyelination enhancement.


Asunto(s)
Ataxia/terapia , Enfermedades Desmielinizantes/terapia , Proteínas de la Membrana/antagonistas & inhibidores , Nanopartículas/química , Proteínas del Tejido Nervioso/antagonistas & inhibidores , Fármacos Neuroprotectores/administración & dosificación , ARN Interferente Pequeño/genética , Remielinización/genética , Administración Intranasal , Animales , Ataxia/inducido químicamente , Ataxia/genética , Ataxia/patología , Caspasa 3/genética , Caspasa 3/metabolismo , Quitosano/química , Enfermedades Desmielinizantes/inducido químicamente , Enfermedades Desmielinizantes/genética , Enfermedades Desmielinizantes/patología , Modelos Animales de Enfermedad , Portadores de Fármacos , Composición de Medicamentos/métodos , Etidio/toxicidad , Regulación de la Expresión Génica , Masculino , Proteínas de la Membrana/genética , Proteínas de la Membrana/metabolismo , Proteína Básica de Mielina/agonistas , Proteína Básica de Mielina/genética , Proteína Básica de Mielina/metabolismo , Vaina de Mielina/metabolismo , Vaina de Mielina/patología , Nanopartículas/administración & dosificación , Proteínas del Tejido Nervioso/genética , Proteínas del Tejido Nervioso/metabolismo , Núcleo Magno del Rafe/efectos de los fármacos , Núcleo Magno del Rafe/metabolismo , Núcleo Magno del Rafe/patología , ARN Interferente Pequeño/metabolismo , Ratas , Ratas Wistar , Técnicas Estereotáxicas
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