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Behav Brain Res ; 329: 104-110, 2017 06 30.
Artículo en Inglés | MEDLINE | ID: mdl-28442361

RESUMEN

Spinal cord injury (SCI) often leads to constant neurological deficits and long-term unalterable disability. Apoptosis plays an important role in the initiation of the secondary injury cascades leading to progressive tissue damage and severely functional deficits after SCI. Although the primary mechanical destructive events cannot be reversed, a therapeutic intervention could be carried out in order to moderate the secondary injury damage several hours to weeks after injury. Astaxanthin (AST) is a strong antioxidant and anti-inflammatory agents with the potential to render anti-apoptotic and neuroprotective effects. In the current study, we examined the therapeutic potential of AST on adult rats after severe SCI contusion. Results of BBB scores showed that AST improved motor function after SCI compared to control groups. Western blot analysis showed reduced expression of Bax and Cleaved-caspase-3 proteins and increased expression of the Bcl-2 protein in response to AST treatment (p<0.05). The histology results also showed that AST considerably preserved myelinated white matter and the number of motor neurons. This study is the first to report that AST reduces neuronal apoptosis, diminishes pathological tissue damage and improves functional recovery after SCI. The observed prominent neuroprotective effects, introduces AST as a promising therapy for SCI.


Asunto(s)
Fármacos Neuroprotectores/uso terapéutico , Traumatismos de la Médula Espinal/tratamiento farmacológico , Animales , Apoptosis/efectos de los fármacos , Modelos Animales de Enfermedad , Locomoción/efectos de los fármacos , Masculino , Neuronas/efectos de los fármacos , Neuronas/patología , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Ratas , Ratas Wistar , Médula Espinal/patología , Traumatismos de la Médula Espinal/patología , Traumatismos de la Médula Espinal/fisiopatología , Factores de Tiempo , Xantófilas/uso terapéutico , Proteína X Asociada a bcl-2/metabolismo
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