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Oxid Med Cell Longev ; 2016: 3173564, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-28090244

RESUMEN

Stroke is a leading cause of death and neurological disability worldwide and striatal ischemic stroke is frequent in humans due to obstruction of middle cerebral artery. Several pathological events underlie damage progression and a comprehensive description of the pathological features following experimental stroke in both acute and chronic survival times is a necessary step for further functional studies. Here, we explored the patterns of microglial activation, astrocytosis, oligodendrocyte damage, myelin impairment, and Nogo-A immunoreactivity between 3 and 30 postlesion days (PLDs) after experimental striatal stroke in adult rats induced by microinjections of endothelin-1 (ET-1). The focal ischemia induced tissue loss concomitant with intense microglia activation between 3 and 14 PLDs (maximum at 7 PLDs), decreasing afterward. Astrocytosis was maximum around 7 PLDs. Oligodendrocyte damage and Nogo-A upregulation were higher at 3 PLDs. Myelin impairment was maximum between 7 and 14 PLDs. Nogo-A expression was higher in the first week in comparison to control. The results add important histopathological features of ET-1 induced stroke in subacute and chronic survival times. In addition, the establishment of the temporal evolution of these neuropathological events is an important step for future studies seeking suitable neuroprotective drugs targeting neuroinflammation and white matter damage.


Asunto(s)
Microglía/metabolismo , Accidente Cerebrovascular/patología , Animales , Astrocitos/citología , Astrocitos/metabolismo , Encéfalo/patología , Isquemia Encefálica/patología , Modelos Animales de Enfermedad , Endotelina-1/toxicidad , Inmunohistoquímica , Masculino , Microglía/citología , Microscopía , Proteína Básica de Mielina/inmunología , Proteína Básica de Mielina/metabolismo , Proteínas Nogo/metabolismo , Oligodendroglía/citología , Oligodendroglía/metabolismo , Ratas , Ratas Wistar , Accidente Cerebrovascular/etiología , Accidente Cerebrovascular/metabolismo , Regulación hacia Arriba/efectos de los fármacos , Sustancia Blanca/metabolismo
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