Efeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratos

Detalhes bibliográficos
Ano de defesa: 2016
Autor(a) principal: Maria Paula Rajao Costa Coelho
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de Minas Gerais
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Ciência animal
Link de acesso: https://hdl.handle.net/1843/SMOC-A82GUH
Resumo: Spinal cord injury is a common disease in human and veterinary medicine, with serious consequences for the one affected and for society. It causes damage to the nervous tissue by primary and secondary mechanisms, being exacerbated influx of calcium, mainly due to the activation voltage-dependent calcium channels, a secondary event considered critical in the pathogenesis of spinal cord injury. The Ph1 peptide obtained from the purification of the whole venom of Phoneutria nigriventer spider is able to block voltage-dependent calcium channels and thereby reduce calcium influx. This study aimed to evaluate the effect of intrathecal administration of different doses of recombinant Ph1 toxin in spinal cord experimentally injured rats. Thirty male Wistar rats were randomly distributed into five groups. Animals belonging to CN group underwent dorsal laminectomy. In other groups, beyond laminectomy, animals underwent acute spinal cord contusive trauma. Animals belonging the control groups received placebo intrathecally administered and treated animals received 25, 50 e 100 pmol of the toxin by the same via. Forty-eight hours after surgery animals were euthanized and were collected blood and urine samples, besides and spinal cord segments, for reactive oxygen species and lipid peroxidation quantification and to assess gene expression of apoptosis- related genes by qRT-PCR. It showed reduction in lipid peroxidation in all three groups who had received the toxin, wich suggests neuroprotector effect.
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spelling 2019-08-11T04:47:12Z2025-09-08T23:22:41Z2019-08-11T04:47:12Z2016-01-28https://hdl.handle.net/1843/SMOC-A82GUHSpinal cord injury is a common disease in human and veterinary medicine, with serious consequences for the one affected and for society. It causes damage to the nervous tissue by primary and secondary mechanisms, being exacerbated influx of calcium, mainly due to the activation voltage-dependent calcium channels, a secondary event considered critical in the pathogenesis of spinal cord injury. The Ph1 peptide obtained from the purification of the whole venom of Phoneutria nigriventer spider is able to block voltage-dependent calcium channels and thereby reduce calcium influx. This study aimed to evaluate the effect of intrathecal administration of different doses of recombinant Ph1 toxin in spinal cord experimentally injured rats. Thirty male Wistar rats were randomly distributed into five groups. Animals belonging to CN group underwent dorsal laminectomy. In other groups, beyond laminectomy, animals underwent acute spinal cord contusive trauma. Animals belonging the control groups received placebo intrathecally administered and treated animals received 25, 50 e 100 pmol of the toxin by the same via. Forty-eight hours after surgery animals were euthanized and were collected blood and urine samples, besides and spinal cord segments, for reactive oxygen species and lipid peroxidation quantification and to assess gene expression of apoptosis- related genes by qRT-PCR. It showed reduction in lipid peroxidation in all three groups who had received the toxin, wich suggests neuroprotector effect.Universidade Federal de Minas GeraisPhoneutria nigriventerperoxidação lipídicaem tempo realespécies reativas de oxigênioqRT-PCRLesão medularapoptoseMascis impactorcálcioCiência animalEfeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratosinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisMaria Paula Rajao Costa Coelhoinfo:eu-repo/semantics/openAccessporreponame:Repositório Institucional da UFMGinstname:Universidade Federal de Minas Gerais (UFMG)instacron:UFMGEliane Goncalves de MeloBenito Soto BlancoNancy Scardua BindaO trauma medular é afecção comum nas medicinas humana e veterinária, com graves consequências para o indívudo acometido e para a sociedade. A lesão à medula espinhal ocasiona dano ao tecido nervoso por mecanismos primários e secundários, sendo o influxo exacerbado de cálcio, principalmente devido à ativação de canais para cálcio voltagem-dependentes (CCVD), um evento secundário considerado crítico na fisiopatogenia da injúria medular. O peptídeo Ph1 obtido da purificação do veneno total da aranha armadeira Phoneutria nigriventer é capaz de bloquear CCVD e, assim, reduzir o influxo de cálcio. Objetivou-se avaliar o efeito da aplicação intratecal de diferentes doses da toxina Ph1 recombinante em ratos submetidos a trauma medular agudo experimental. Foram utilizados 30 ratos machos adultos, variedade Wistar, aleatoriamente divididos em cinco grupos. Os animais do grupo CN foram submetidos à laminectomia dorsal. Nos demais grupos, além da laminectomia, os animais foram submetidos à trauma medular agudo contusivo. Realizou-se aplicação intratecal de placebo nos animais dos grupos controle e das doses de 25,50 e 100 pmol da toxina Ph1 recombinante nos animais tratados. 48 horas após a intervenção cirúrgica, os animais foram eutanasiados e foram coletadas amostras de sangue, urina e segmentos de medula espinhal, para quantificação de espécies reativas de oxigênio e peroxidação lipídica e avaliação da expressão gênica de fatores relacionados à apoptose através de técnica de qRT-PCR. Observou-se redução de peroxidação lípica nos três grupos submetidos ao tratamento, o que sugere ação neuroprotetora desta toxina.UFMGORIGINALdisserta__o_maria_paula_raj_o_costa_coelho.pdfapplication/pdf1463758https://repositorio.ufmg.br//bitstreams/b6032a80-9c1e-4f4a-b629-313a1bb0faad/download72ab7119e0a22b5bd8857b2f3b2f4521MD51trueAnonymousREADTEXTdisserta__o_maria_paula_raj_o_costa_coelho.pdf.txttext/plain166774https://repositorio.ufmg.br//bitstreams/2aa9ad7c-b081-4a27-bcdd-63b0e168dc3f/downloadbe01e485ef8569c0afe1d9cb7ae458ecMD52falseAnonymousREAD1843/SMOC-A82GUH2025-09-08 20:22:41.523open.accessoai:repositorio.ufmg.br:1843/SMOC-A82GUHhttps://repositorio.ufmg.br/Repositório InstitucionalPUBhttps://repositorio.ufmg.br/oairepositorio@ufmg.bropendoar:2025-09-08T23:22:41Repositório Institucional da UFMG - Universidade Federal de Minas Gerais (UFMG)false
dc.title.none.fl_str_mv Efeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratos
title Efeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratos
spellingShingle Efeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratos
Maria Paula Rajao Costa Coelho
Ciência animal
Phoneutria nigriventer
peroxidação lipídica
em tempo real
espécies reativas de oxigênio
qRT-PCR
Lesão medular
apoptose
Mascis impactor
cálcio
title_short Efeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratos
title_full Efeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratos
title_fullStr Efeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratos
title_full_unstemmed Efeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratos
title_sort Efeito neuroprotetor da toxina Ph 1 recombinante no trauma medular agudo em ratos
author Maria Paula Rajao Costa Coelho
author_facet Maria Paula Rajao Costa Coelho
author_role author
dc.contributor.author.fl_str_mv Maria Paula Rajao Costa Coelho
dc.subject.por.fl_str_mv Ciência animal
topic Ciência animal
Phoneutria nigriventer
peroxidação lipídica
em tempo real
espécies reativas de oxigênio
qRT-PCR
Lesão medular
apoptose
Mascis impactor
cálcio
dc.subject.other.none.fl_str_mv Phoneutria nigriventer
peroxidação lipídica
em tempo real
espécies reativas de oxigênio
qRT-PCR
Lesão medular
apoptose
Mascis impactor
cálcio
description Spinal cord injury is a common disease in human and veterinary medicine, with serious consequences for the one affected and for society. It causes damage to the nervous tissue by primary and secondary mechanisms, being exacerbated influx of calcium, mainly due to the activation voltage-dependent calcium channels, a secondary event considered critical in the pathogenesis of spinal cord injury. The Ph1 peptide obtained from the purification of the whole venom of Phoneutria nigriventer spider is able to block voltage-dependent calcium channels and thereby reduce calcium influx. This study aimed to evaluate the effect of intrathecal administration of different doses of recombinant Ph1 toxin in spinal cord experimentally injured rats. Thirty male Wistar rats were randomly distributed into five groups. Animals belonging to CN group underwent dorsal laminectomy. In other groups, beyond laminectomy, animals underwent acute spinal cord contusive trauma. Animals belonging the control groups received placebo intrathecally administered and treated animals received 25, 50 e 100 pmol of the toxin by the same via. Forty-eight hours after surgery animals were euthanized and were collected blood and urine samples, besides and spinal cord segments, for reactive oxygen species and lipid peroxidation quantification and to assess gene expression of apoptosis- related genes by qRT-PCR. It showed reduction in lipid peroxidation in all three groups who had received the toxin, wich suggests neuroprotector effect.
publishDate 2016
dc.date.issued.fl_str_mv 2016-01-28
dc.date.accessioned.fl_str_mv 2019-08-11T04:47:12Z
2025-09-08T23:22:41Z
dc.date.available.fl_str_mv 2019-08-11T04:47:12Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/masterThesis
format masterThesis
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://hdl.handle.net/1843/SMOC-A82GUH
url https://hdl.handle.net/1843/SMOC-A82GUH
dc.language.iso.fl_str_mv por
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dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv Universidade Federal de Minas Gerais
publisher.none.fl_str_mv Universidade Federal de Minas Gerais
dc.source.none.fl_str_mv reponame:Repositório Institucional da UFMG
instname:Universidade Federal de Minas Gerais (UFMG)
instacron:UFMG
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institution UFMG
reponame_str Repositório Institucional da UFMG
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