Please use this identifier to cite or link to this item: http://www.repositorio.ufop.br/handle/123456789/11071
Title: Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.
Authors: Oliveira, Karen Maciel de
Binda, Nancy Scardua
Lavor, Mário Sérgio Lima de
Silva, Carla Maria Osório
Rosado, Isabel Rodrigues
Alves, Endrigo Gabellini Leonel
Silva, Juliana Figueira da
Oliveira, Camila M.
Melo, Marilia Martins
Gomez, Marcus Vinicius
Melo, Eliane Gonçalves de
Issue Date: 2018
Citation: OLIVEIRA, 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.
Abstract: This 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.
URI: http://www.repositorio.ufop.br/handle/123456789/11071
ISSN: 1935-2735
metadata.dc.rights.license: This 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.
Appears in Collections:DEFAR - Artigos publicados em periódicos

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