Guanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratos
Autor(a) principal: | |
---|---|
Data de Publicação: | 2016 |
Tipo de documento: | Dissertação |
Idioma: | por |
Título da fonte: | Repositório Institucional Manancial UFSM |
Texto Completo: | http://repositorio.ufsm.br/handle/1/18024 |
Resumo: | Traumatic brain injury (TBI) affects annually 10 million of people causing neurological symptoms and deaths resulting in an adverse socio-economic impact worldwide. The pathophysiology of TBI comprises multiple neurotoxic processes, such as excitotoxicity, mitochondrial dysfunction and inflammation leading to neuronal death and consequently clinical manifestations, as motor deficit. Many studies with promising drugs in experimental models of TBI reported failures in clinical tests, so it is important to search for new therapeutic drugs. Currently, much attention has been devoted to the neuroprotective effects of guanosine, an endogenous nucleoside able to reduce neurotoxic events in experimental models of ischemia in vivo and in vitro, which to our knowledge has not yet been evaluated in the TBI. Therefore, the present study evaluated the therapeutic potential of guanosine in locomotor impairment and neurodegeneration after TBI by controlling excitotoxicity, mitochondrial and inflammatory alterations. Male Wistar rats were subjected to TBI by moderate fluid percussion injury (PFS) parasagittal model and 40 minutes after was administered guanosine (7.5mg / kg intraperitoneally). Our results show that guanosine protects against the locomotor deficit induced by TBI 8 hours after the insult. Similarly, guanosine was also able to protect against the neurochemical damage in the ipsilateral cortex characterized by the inhibition of glutamate uptake, Na+, K+ - ATPase and glutamine synthetase activity , alterations in mitochondrial membrane potential (ΔѰm) followed by an increase in production of reactive species oxygen (ROS) and content of protein carbonyls. Furthermore, the inflammatory response induced by TBI evidenced by increased levels of TNF-α, IL-1β and cerebral edema was also reduced by guanosine. In addition to these findings, guanosine protected against the neuronal death and activation of caspase 3, reinforcing its neuroprotective effects. Thus, our study represents an important contribution to the knowledge of the neuroprotective effects of guanosine in the TBI, making this an attractive candidate molecule for the treatment of this insult, although more studies are needed to clarify their potential in clinical TBI. |
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2019-08-26T18:45:44Z2019-08-26T18:45:44Z2016-01-29http://repositorio.ufsm.br/handle/1/18024Traumatic brain injury (TBI) affects annually 10 million of people causing neurological symptoms and deaths resulting in an adverse socio-economic impact worldwide. The pathophysiology of TBI comprises multiple neurotoxic processes, such as excitotoxicity, mitochondrial dysfunction and inflammation leading to neuronal death and consequently clinical manifestations, as motor deficit. Many studies with promising drugs in experimental models of TBI reported failures in clinical tests, so it is important to search for new therapeutic drugs. Currently, much attention has been devoted to the neuroprotective effects of guanosine, an endogenous nucleoside able to reduce neurotoxic events in experimental models of ischemia in vivo and in vitro, which to our knowledge has not yet been evaluated in the TBI. Therefore, the present study evaluated the therapeutic potential of guanosine in locomotor impairment and neurodegeneration after TBI by controlling excitotoxicity, mitochondrial and inflammatory alterations. Male Wistar rats were subjected to TBI by moderate fluid percussion injury (PFS) parasagittal model and 40 minutes after was administered guanosine (7.5mg / kg intraperitoneally). Our results show that guanosine protects against the locomotor deficit induced by TBI 8 hours after the insult. Similarly, guanosine was also able to protect against the neurochemical damage in the ipsilateral cortex characterized by the inhibition of glutamate uptake, Na+, K+ - ATPase and glutamine synthetase activity , alterations in mitochondrial membrane potential (ΔѰm) followed by an increase in production of reactive species oxygen (ROS) and content of protein carbonyls. Furthermore, the inflammatory response induced by TBI evidenced by increased levels of TNF-α, IL-1β and cerebral edema was also reduced by guanosine. In addition to these findings, guanosine protected against the neuronal death and activation of caspase 3, reinforcing its neuroprotective effects. Thus, our study represents an important contribution to the knowledge of the neuroprotective effects of guanosine in the TBI, making this an attractive candidate molecule for the treatment of this insult, although more studies are needed to clarify their potential in clinical TBI.O traumatismo cranioencefálico (TCE) afeta anualmente 10 milhões de pessoas ocasionando mortes e sintomas neurológicos que resultam em um impacto socioeconômico desfavorável a nível mundial. Sua fisiopatologia compreende múltiplos processos neurotóxicos, tais como a excitotoxicidade, disfunção mitocondrial e inflamação que conduzem a morte neuronal e, consequentemente a manifestações clínicas, como o déficit motor. Muitos estudos com drogas promissoras em modelos experimentais de TCE reportaram falhas quando testadas clinicamente, assim torna-se importante à busca por novas drogas terapêuticas. Atualmente, muita atenção tem sido dedicada aos efeitos neuroprotetores da guanosina, um nucleosídeo endógeno capaz de reduzir eventos neurotóxicos em modelos experimentais de isquemia in vivo e in vitro, que ao nosso conhecimento, ainda não foi avaliada no TCE. Portanto, o presente estudo avaliou o potencial terapêutico da guanosina no prejuízo locomotor e neurodegeneração após o TCE por controlar a excitotoxicidade, alterações mitocondriais e inflamatórias. Ratos Wistar machos foram submetidos ao TCE pelo modelo de lesão por percussão de fluido sagital (PFS) e 40 minutos após foi administrado guanosina na dose 7.5mg/kg via intraperitoneal ( i.p). Nossos resultados revelam que a guanosina protege contra o prejuízo locomotor induzido pelo PFS 8 horas após o insulto. Do mesmo modo, a guanosina também foi capaz de proteger contra o dano neuroquímico no córtex ipsilateral caracterizado pela inibição da captação de glutamato, Na+, K+ - ATPase e glutamina sintetase, alterações do potencial de membrana mitocondrial (ΔѰm) seguido pela produção de espécies reativas de oxigênio (ERO) e aumento no conteúdo de proteínas carboniladas. De forma semelhante, a resposta inflamatória induzida pelo PFS evidenciada pelo aumento nos níveis de TNF- α, IL-1β e edema cerebral também foi reduzida por esse nucleosídeo. Além destas descobertas, a guanosina protegeu contra a morte neuronal e ativação da caspase 3, reforçando seus efeitos neuroprotetores. Dessa forma, o nosso estudo representa uma importante contribuição para o conhecimento dos efeitos neuroprotetores da guanosina no TCE, tornando esta molécula uma atraente candidata para o tratamento desse insulto, embora mais estudos sejam necessários para esclarecer o seu potencial clinico no TCE.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPESporUniversidade Federal de Santa MariaCentro de Ciências Naturais e ExatasPrograma de Pós-Graduação em Ciências Biológicas: Bioquímica ToxicológicaUFSMBrasilBioquímicaAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessTraumatismo cranioencefálicoExitotoxicidadeMitocôndriaInflamaçãoDéficit motorGuanosinaRatosTraumatic brain injuryExitotoxicityMitochondriaInflammationMotor deficitGuanosineRatsCNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICAGuanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratosGuanosine reduces the neurotoxicity and the motor deficit induced by traumatic brain injury in ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisRoyes, Luiz Fernando Freirehttp://lattes.cnpq.br/0543081555633400Puntel, Gustavo Orionehttp://lattes.cnpq.br/0319301096075015http://lattes.cnpq.br/2036124245207167Gerbatin, Rogério da Rosa200800000002600c83ec235-e54e-44ae-bea7-573d588ca1838da110e4-2c93-441d-bb6b-fbee027f45ca88aca416-9efe-4fc1-9d1b-46476590ef15reponame:Repositório Institucional Manancial UFSMinstname:Universidade Federal de Santa Maria (UFSM)instacron:UFSMCC-LICENSElicense_rdflicense_rdfapplication/rdf+xml; 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dc.title.por.fl_str_mv |
Guanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratos |
dc.title.alternative.eng.fl_str_mv |
Guanosine reduces the neurotoxicity and the motor deficit induced by traumatic brain injury in rats |
title |
Guanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratos |
spellingShingle |
Guanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratos Gerbatin, Rogério da Rosa Traumatismo cranioencefálico Exitotoxicidade Mitocôndria Inflamação Déficit motor Guanosina Ratos Traumatic brain injury Exitotoxicity Mitochondria Inflammation Motor deficit Guanosine Rats CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA |
title_short |
Guanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratos |
title_full |
Guanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratos |
title_fullStr |
Guanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratos |
title_full_unstemmed |
Guanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratos |
title_sort |
Guanonisa reduz a neurotoxicidade e o déficit motor induzido pelo traumatismo cranioencefálico em ratos |
author |
Gerbatin, Rogério da Rosa |
author_facet |
Gerbatin, Rogério da Rosa |
author_role |
author |
dc.contributor.advisor1.fl_str_mv |
Royes, Luiz Fernando Freire |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/0543081555633400 |
dc.contributor.referee1.fl_str_mv |
Puntel, Gustavo Orione |
dc.contributor.referee1Lattes.fl_str_mv |
http://lattes.cnpq.br/0319301096075015 |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/2036124245207167 |
dc.contributor.author.fl_str_mv |
Gerbatin, Rogério da Rosa |
contributor_str_mv |
Royes, Luiz Fernando Freire Puntel, Gustavo Orione |
dc.subject.por.fl_str_mv |
Traumatismo cranioencefálico Exitotoxicidade Mitocôndria Inflamação Déficit motor Guanosina Ratos |
topic |
Traumatismo cranioencefálico Exitotoxicidade Mitocôndria Inflamação Déficit motor Guanosina Ratos Traumatic brain injury Exitotoxicity Mitochondria Inflammation Motor deficit Guanosine Rats CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA |
dc.subject.eng.fl_str_mv |
Traumatic brain injury Exitotoxicity Mitochondria Inflammation Motor deficit Guanosine Rats |
dc.subject.cnpq.fl_str_mv |
CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA |
description |
Traumatic brain injury (TBI) affects annually 10 million of people causing neurological symptoms and deaths resulting in an adverse socio-economic impact worldwide. The pathophysiology of TBI comprises multiple neurotoxic processes, such as excitotoxicity, mitochondrial dysfunction and inflammation leading to neuronal death and consequently clinical manifestations, as motor deficit. Many studies with promising drugs in experimental models of TBI reported failures in clinical tests, so it is important to search for new therapeutic drugs. Currently, much attention has been devoted to the neuroprotective effects of guanosine, an endogenous nucleoside able to reduce neurotoxic events in experimental models of ischemia in vivo and in vitro, which to our knowledge has not yet been evaluated in the TBI. Therefore, the present study evaluated the therapeutic potential of guanosine in locomotor impairment and neurodegeneration after TBI by controlling excitotoxicity, mitochondrial and inflammatory alterations. Male Wistar rats were subjected to TBI by moderate fluid percussion injury (PFS) parasagittal model and 40 minutes after was administered guanosine (7.5mg / kg intraperitoneally). Our results show that guanosine protects against the locomotor deficit induced by TBI 8 hours after the insult. Similarly, guanosine was also able to protect against the neurochemical damage in the ipsilateral cortex characterized by the inhibition of glutamate uptake, Na+, K+ - ATPase and glutamine synthetase activity , alterations in mitochondrial membrane potential (ΔѰm) followed by an increase in production of reactive species oxygen (ROS) and content of protein carbonyls. Furthermore, the inflammatory response induced by TBI evidenced by increased levels of TNF-α, IL-1β and cerebral edema was also reduced by guanosine. In addition to these findings, guanosine protected against the neuronal death and activation of caspase 3, reinforcing its neuroprotective effects. Thus, our study represents an important contribution to the knowledge of the neuroprotective effects of guanosine in the TBI, making this an attractive candidate molecule for the treatment of this insult, although more studies are needed to clarify their potential in clinical TBI. |
publishDate |
2016 |
dc.date.issued.fl_str_mv |
2016-01-29 |
dc.date.accessioned.fl_str_mv |
2019-08-26T18:45:44Z |
dc.date.available.fl_str_mv |
2019-08-26T18:45:44Z |
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info:eu-repo/semantics/publishedVersion |
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info:eu-repo/semantics/masterThesis |
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masterThesis |
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http://repositorio.ufsm.br/handle/1/18024 |
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http://repositorio.ufsm.br/handle/1/18024 |
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por |
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por |
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200800000002 |
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600 |
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Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ info:eu-repo/semantics/openAccess |
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Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ |
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openAccess |
dc.publisher.none.fl_str_mv |
Universidade Federal de Santa Maria Centro de Ciências Naturais e Exatas |
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Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica |
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UFSM |
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Brasil |
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Bioquímica |
publisher.none.fl_str_mv |
Universidade Federal de Santa Maria Centro de Ciências Naturais e Exatas |
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