Ômega-conotoxina MVIIC no trauma experimental da medula espinhal.

• Ano de defesa: 2017
• Autor(a) principal: Juan Sebastian Gutierrez Lozano
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; Brasil; VET - DEPARTAMENTO DE CLÍNICA E CIRURGIA; Programa de Pós-Graduação em Ciência Animal; UFMG
• Palavras-chave em Português: Trauma Medular; Neuroproteção; Ômega-conotoxina MVIIC; Cálcio; Apoptose; Peroxidação Lipídica; Espécies Reativas de Oxigênio; Trauma medular
• Link de acesso: http://hdl.handle.net/1843/31553

Spinal cord trauma is a common condition in veterinary medicine. It can lead to serious consequences such as deficits in sensory and autonomic motor function for the affected animal and can determine the euthanasia of the affected animal. Marrow lesions cause damage to nerve tissue by primary and secondary mechanisms. The primary and irreversible lesion, already in the secondary mechanism an exacerbated influx of calcium is produced, mainly due to the activation of voltage-dependent calcium channels (CCVD). This event is considered critical in the pathophysiology of spinal cord injury. The Omega-conotoxin MVIIC obtained from the purification of the venom of Conus magus is able to block CCVD and thus reduce the influx of calcium. The present study evaluated the effect of intrathecal application of omega-conotoxin MVIIC at doses 15 and 30 pmol and at the times 5 minutes and one hour after the experimental bone marrow trauma in rats. Thirty - six adult male Wistar rats were randomly divided into six groups. The animals of the Negative Control (CN) group were submitted to dorsal laminectomy. In the other groups, in addition to laminectomy, the animals were submitted to acute medullary trauma by the device MASCIS impactor. Intrathecal application of placebo was performed in the animals of the Positive Control (CP) groups. In Groups G3 and G5 doses of 15 and 30 pmol, respectively, of the Omega-conotoxin toxin MVIIC, were applied in the treated animals 5 minutes after the trauma. In Groups G4 and G6 doses of 15 and 30, respectively, were applied one hour after the trauma. The animals were euthanized 48 hours after the surgical intervention and the application of the toxin. Finally, blood samples were collected to evaluate the side effects and spinal cord segments for the quantification of reactive oxygen species and lipid peroxidation and for the evaluation of the gene expression of factors related to apoptosis by means of the qRTPCR. There was a reduction in ROS production in the treated group at 15 pmol / 5 minutes post trauma, suggesting a tendency to reduce ROS levels, which would probably be related to the reduction of the pathogenic events due to the intracellular accumulation of calcium by blocking CCVD.