Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.

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dc.contributor.authorOliveira, Karen Maciel de
dc.contributor.authorBinda, Nancy Scardua
dc.contributor.authorLavor, Mário Sérgio Lima de
dc.contributor.authorSilva, Carla Maria Osório
dc.contributor.authorRosado, Isabel Rodrigues
dc.contributor.authorAlves, Endrigo Gabellini Leonel
dc.contributor.authorSilva, Juliana Figueira da
dc.contributor.authorOliveira, Camila M.
dc.contributor.authorMelo, Marilia Martins
dc.contributor.authorGomez, Marcus Vinicius
dc.contributor.authorMelo, Eliane Gonçalves de
dc.date.accessioned2019-04-22T11:17:07Z
dc.date.available2019-04-22T11:17:07Z
dc.date.issued2018
dc.description.abstractThis study evaluates whether intrathecal MVIIA injection after spinal cord injury (SCI) elicits neuroprotective effects. The test rats were randomly distributed into six groups— sham, placebo, MVIIA 2.5 μM, MVIIA 5 μM, MVIIA 10 μM, and MVIIA 20 μM—and were administered the treatment four hours after SCI. After the optimal MVIIA dose (MVIIA 10 μM) was defined, the best time for application, one or four hours, was analyzed. Locomotor hind limb function and side effects were assessed. Forty-eight hours after the injury and immediately after euthanasia, spinal cord segments were removed from the test rats. Cell viability, reactive oxygen species, lipid peroxidation, and glutamate release were investigated. To examine the MVIIA mechanism of action, the gene expressions of pro-apoptotic (Bax, nNOS, and caspase-3, -8, -9, -12) and anti-apoptotic (Bcl-xl) factors in the spinal cord tissue samples were determined by real-time PCR, and the activities of antioxidant enzymes were also investigated. Application of intrathecal MVIIA 10 μM four hours after SCI prompted a neuroprotective effect: neuronal death decreased (22.46%), oxidative stress diminished, pro-apoptotic factors (Bax, nNOS, and caspase-3, -8) were expressed to a lesser extent, and mitochondrial viability as well as anti-apoptotic factor (Bcl-xl) expression increased. These results suggested that MVIIA provided neuroprotection through antioxidant effects. Indeed, superoxide dismutase (188.41%), and glutathione peroxidase (199.96%), reductase (193.86%), and transferase (175.93%) expressions increased. Therefore, intrathecal MVIIA (MVIIA 10 μM, 4 h) application has neuroprotective potential, and the possible mechanisms are related to antioxidant agent modulation and to intrinsic and extrinsic apoptotic pathways.pt_BR
dc.identifier.citationOLIVEIRA, K. M. de et al. Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats. PLoS One, v. 13, n. 10, p. 1-26, out. 2018. Disponível em: <https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0204948>. Acesso em: 25 fev. 2019.pt_BR
dc.identifier.issn1935-2735
dc.identifier.urihttp://www.repositorio.ufop.br/handle/123456789/11071
dc.language.isoen_USpt_BR
dc.rightsabertopt_BR
dc.rights.licenseThis is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Fonte: o próprio artigo.pt_BR
dc.titleConotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.pt_BR
dc.typeArtigo publicado em periodicopt_BR
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