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

Detalhes bibliográficos
Autor(a) principal: Oliveira, Karen Maciel de
Data de Publicação: 2018
Outros Autores: 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
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFOP
Texto Completo: http://www.repositorio.ufop.br/handle/123456789/11071
Resumo: 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.
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spelling Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.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.2019-04-22T11:17:07Z2019-04-22T11:17:07Z2018info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfOLIVEIRA, 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. 2019.1935-2735http://www.repositorio.ufop.br/handle/123456789/11071This 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.info:eu-repo/semantics/openAccessOliveira, Karen Maciel deBinda, Nancy ScarduaLavor, Mário Sérgio Lima deSilva, Carla Maria OsórioRosado, Isabel RodriguesAlves, Endrigo Gabellini LeonelSilva, Juliana Figueira daOliveira, Camila M.Melo, Marilia MartinsGomez, Marcus ViniciusMelo, Eliane Gonçalves deengreponame:Repositório Institucional da UFOPinstname:Universidade Federal de Ouro Preto (UFOP)instacron:UFOP2019-04-22T11:17:07Zoai:repositorio.ufop.br:123456789/11071Repositório InstitucionalPUBhttp://www.repositorio.ufop.br/oai/requestrepositorio@ufop.edu.bropendoar:32332019-04-22T11:17:07Repositório Institucional da UFOP - Universidade Federal de Ouro Preto (UFOP)false
dc.title.none.fl_str_mv Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.
title Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.
spellingShingle Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.
Oliveira, Karen Maciel de
title_short Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.
title_full Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.
title_fullStr Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.
title_full_unstemmed Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.
title_sort Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.
author Oliveira, Karen Maciel de
author_facet 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
author_role author
author2 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
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv 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
description 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.
publishDate 2018
dc.date.none.fl_str_mv 2018
2019-04-22T11:17:07Z
2019-04-22T11:17:07Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv 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.
1935-2735
http://www.repositorio.ufop.br/handle/123456789/11071
identifier_str_mv 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.
1935-2735
url http://www.repositorio.ufop.br/handle/123456789/11071
dc.language.iso.fl_str_mv eng
language eng
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:Repositório Institucional da UFOP
instname:Universidade Federal de Ouro Preto (UFOP)
instacron:UFOP
instname_str Universidade Federal de Ouro Preto (UFOP)
instacron_str UFOP
institution UFOP
reponame_str Repositório Institucional da UFOP
collection Repositório Institucional da UFOP
repository.name.fl_str_mv Repositório Institucional da UFOP - Universidade Federal de Ouro Preto (UFOP)
repository.mail.fl_str_mv repositorio@ufop.edu.br
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