Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimer

Detalhes bibliográficos
Autor(a) principal: Ibarra, Diany Gisela Arcos
Data de Publicação: 2020
Tipo de documento: Dissertação
Idioma: por
Título da fonte: Repositório do Centro Universitário Braz Cubas
Texto Completo: https://repositorio.cruzeirodosul.edu.br/handle/123456789/2299
Resumo: Alzheimer's disease (AD) is a progressive neurodegenerative disorder and is the leading cause of dementia in late adulthood. Histopathologically, it is characterized by intracellular neurofibrillary tangles and deposits of extracellular amyloid beta protein that contribute to the formation of senile plaques. Several risk factors are associated with AD, triggering neuroinflammation, oxidative stress and cognitive impairment. While the neuropathological features of Alzheimer's disease are recognized, the complexities of the mechanisms associated with its onset and progression have not been clearly elucidated. The aim of the present research was to evaluate the expression of TNF (Tumor Necrosis Factor), CX3CR1 (Chemokine Receptor 1) and TREM2 (Triggering Receptor Expressed on Myeloid cells 2) genes in a model of streptozotocin (STZ) intracerebroventricular (icv) induced neurodegeneration. For this, 20 male Wistar rats were divided into four experimental groups: Group 1 (n = 5, control group 1), composed of animals with icv citrate buffer injection and euthanized 1 month after citrate buffer administration; Group 2 (n = 5), group composed of animals that received STZ via icv, also euthanized after 1 month of neurodegeneration induction; Group 3 (n = 5, control group 2), group that received icv citrate buffer and were euthanized after 4 months of icv administration; Group 4 (n = 5), group that received STZ via icv and were euthanized after 4 months of STZ administration. After euthanasia, the animals had their hippocampus removed for RNA extraction. Total RNA extracted from these samples was converted to cDNA by reverse transcription reaction. Subsequently, the samples will be subjected to quantitative polymerase chain reaction (qPCR) for analyze of TNF, CX3CR1 and TREM2 gene expression. Expression analysis showed increased expression of the TNF gene in animals that were euthanized after 1 month of neurodegeneration induction. Increased expression of the CX3CR1 gene was also found, however, increased expression of this gene was only seen in the group of euthanized animals after 4 months of the icv administration of STZ. These results indicate an association of neuroinflammation with the development and progression of neurodegenerative processes.
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spelling Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimerBiotecnologiaDemênciaEstreptozocinaCNPQ::CIENCIAS BIOLOGICAS::BIOLOGIA GERALAlzheimer's disease (AD) is a progressive neurodegenerative disorder and is the leading cause of dementia in late adulthood. Histopathologically, it is characterized by intracellular neurofibrillary tangles and deposits of extracellular amyloid beta protein that contribute to the formation of senile plaques. Several risk factors are associated with AD, triggering neuroinflammation, oxidative stress and cognitive impairment. While the neuropathological features of Alzheimer's disease are recognized, the complexities of the mechanisms associated with its onset and progression have not been clearly elucidated. The aim of the present research was to evaluate the expression of TNF (Tumor Necrosis Factor), CX3CR1 (Chemokine Receptor 1) and TREM2 (Triggering Receptor Expressed on Myeloid cells 2) genes in a model of streptozotocin (STZ) intracerebroventricular (icv) induced neurodegeneration. For this, 20 male Wistar rats were divided into four experimental groups: Group 1 (n = 5, control group 1), composed of animals with icv citrate buffer injection and euthanized 1 month after citrate buffer administration; Group 2 (n = 5), group composed of animals that received STZ via icv, also euthanized after 1 month of neurodegeneration induction; Group 3 (n = 5, control group 2), group that received icv citrate buffer and were euthanized after 4 months of icv administration; Group 4 (n = 5), group that received STZ via icv and were euthanized after 4 months of STZ administration. After euthanasia, the animals had their hippocampus removed for RNA extraction. Total RNA extracted from these samples was converted to cDNA by reverse transcription reaction. Subsequently, the samples will be subjected to quantitative polymerase chain reaction (qPCR) for analyze of TNF, CX3CR1 and TREM2 gene expression. Expression analysis showed increased expression of the TNF gene in animals that were euthanized after 1 month of neurodegeneration induction. Increased expression of the CX3CR1 gene was also found, however, increased expression of this gene was only seen in the group of euthanized animals after 4 months of the icv administration of STZ. These results indicate an association of neuroinflammation with the development and progression of neurodegenerative processes.A Doença de Alzheimer (DA) é um distúrbio neurodegenerativo progressivo, sendo a principal causa de demência no final da vida adulta. Histopatologicamente, caracteriza-se por emaranhados neurofibrilares intracelulares e depósitos de proteína beta amilóide extracelular que contribuem para a formação das placas senis. Diversos fatores de risco estão associados à DA, conduzindo à neuroinflamação, aumento do estresse oxidativo e comprometimento cognitivo. Enquanto as características neuropatológicas da doença de Alzheimer são conhecidas, a complexidade dos mecanismos moleculares associados ao seu início e progressão não foi claramente elucidada. O objetivo da presente pesquisa foi avaliar a expressão dos genes TNF (do inglês Tumor Necrosis Factor), CX3CR1 (do inglês Chemokine Receptor 1) e TREM2 (do inglês Triggering Receptor Expressed on Myeloid cells 2) em um modelo de neurodegeneração induzida pela administração intracerebroventricular (icv) de estreptozotocina (STZ). Para isso, foram utilizados 20 ratos machos da linhagem Wistar divididos em quatro grupos experimentais: Grupo 1 (n=5, grupo controle 1), composto por animais que tiveram a administração icv de tampão citrato e eutanasiados após 1 mês da injeção icv; Grupo 2 (n=5, grupo STZ 1), grupo composto por animais que receberam STZ via icv, também eutanasiados após 1 mês da indução da neurodegeneração; Grupo 3 (n=5, grupo controle 2), grupo que recebeu tampão citrato icv e os animais foram eutanasiados após 4 meses da administração icv; Grupo 4 (n=5, grupo STZ 2), grupo que recebeu STZ via icv e os animais foram eutanasiados após 4 meses da administração de STZ. Após a eutanásia, os animais tiveram o hipocampo removido para a extração do RNA. O RNA total extraído foi convertido em cDNA por meio da reação de transcrição reversa. Na sequência, as amostras foram submetidas à reação em cadeia da polimerase quantitativa (qPCR) para análise da expressão dos genes TNF, CX3CR1 e TREM2. A análise de expressão demonstrou aumento da expressão do gene TNF nos animais que foram eutanasiados após 1 mês da indução da neurodegeneração. Também foi encontrado aumento da expressão do gene CX3CR1, entretanto, o aumento da expressão deste gene só foi verificado no grupo de animais eutanasiados após 4 meses da administração icv de STZ. Estes resultados indicam uma participação da neuroinflamação com o desenvolvimento e progressão dos processos neurodegenerativos.Universidade PositivoBrasilPós-GraduaçãoPrograma de Pós-Graduação em Biotecnologia IndustrialUPPincerati, Márciahttp://lattes.cnpq.br/1632493068360047Ibarra, Diany Gisela Arcos2021-05-28T18:45:20Z20202021-05-28T18:45:20Z2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisapplication/pdfhttps://repositorio.cruzeirodosul.edu.br/handle/123456789/2299porinfo:eu-repo/semantics/openAccessreponame:Repositório do Centro Universitário Braz Cubasinstname:Centro Universitário Braz Cubas (CUB)instacron:CUB2021-05-29T11:19:36Zoai:repositorio.cruzeirodosul.edu.br:123456789/2299Repositório InstitucionalPUBhttps://repositorio.brazcubas.edu.br/oai/requestbibli@brazcubas.edu.bropendoar:2021-05-29T11:19:36Repositório do Centro Universitário Braz Cubas - Centro Universitário Braz Cubas (CUB)false
dc.title.none.fl_str_mv Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimer
title Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimer
spellingShingle Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimer
Ibarra, Diany Gisela Arcos
Biotecnologia
Demência
Estreptozocina
CNPQ::CIENCIAS BIOLOGICAS::BIOLOGIA GERAL
title_short Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimer
title_full Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimer
title_fullStr Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimer
title_full_unstemmed Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimer
title_sort Análise da expressão dos genes TNF, CX3CR1 e TREM2 em um modelo animal de neurodegeneração para a doença de alzheimer
author Ibarra, Diany Gisela Arcos
author_facet Ibarra, Diany Gisela Arcos
author_role author
dc.contributor.none.fl_str_mv Pincerati, Márcia
http://lattes.cnpq.br/1632493068360047
dc.contributor.author.fl_str_mv Ibarra, Diany Gisela Arcos
dc.subject.por.fl_str_mv Biotecnologia
Demência
Estreptozocina
CNPQ::CIENCIAS BIOLOGICAS::BIOLOGIA GERAL
topic Biotecnologia
Demência
Estreptozocina
CNPQ::CIENCIAS BIOLOGICAS::BIOLOGIA GERAL
description Alzheimer's disease (AD) is a progressive neurodegenerative disorder and is the leading cause of dementia in late adulthood. Histopathologically, it is characterized by intracellular neurofibrillary tangles and deposits of extracellular amyloid beta protein that contribute to the formation of senile plaques. Several risk factors are associated with AD, triggering neuroinflammation, oxidative stress and cognitive impairment. While the neuropathological features of Alzheimer's disease are recognized, the complexities of the mechanisms associated with its onset and progression have not been clearly elucidated. The aim of the present research was to evaluate the expression of TNF (Tumor Necrosis Factor), CX3CR1 (Chemokine Receptor 1) and TREM2 (Triggering Receptor Expressed on Myeloid cells 2) genes in a model of streptozotocin (STZ) intracerebroventricular (icv) induced neurodegeneration. For this, 20 male Wistar rats were divided into four experimental groups: Group 1 (n = 5, control group 1), composed of animals with icv citrate buffer injection and euthanized 1 month after citrate buffer administration; Group 2 (n = 5), group composed of animals that received STZ via icv, also euthanized after 1 month of neurodegeneration induction; Group 3 (n = 5, control group 2), group that received icv citrate buffer and were euthanized after 4 months of icv administration; Group 4 (n = 5), group that received STZ via icv and were euthanized after 4 months of STZ administration. After euthanasia, the animals had their hippocampus removed for RNA extraction. Total RNA extracted from these samples was converted to cDNA by reverse transcription reaction. Subsequently, the samples will be subjected to quantitative polymerase chain reaction (qPCR) for analyze of TNF, CX3CR1 and TREM2 gene expression. Expression analysis showed increased expression of the TNF gene in animals that were euthanized after 1 month of neurodegeneration induction. Increased expression of the CX3CR1 gene was also found, however, increased expression of this gene was only seen in the group of euthanized animals after 4 months of the icv administration of STZ. These results indicate an association of neuroinflammation with the development and progression of neurodegenerative processes.
publishDate 2020
dc.date.none.fl_str_mv 2020
2020
2021-05-28T18:45:20Z
2021-05-28T18:45:20Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/masterThesis
format masterThesis
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dc.identifier.uri.fl_str_mv https://repositorio.cruzeirodosul.edu.br/handle/123456789/2299
url https://repositorio.cruzeirodosul.edu.br/handle/123456789/2299
dc.language.iso.fl_str_mv por
language por
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.publisher.none.fl_str_mv Universidade Positivo
Brasil
Pós-Graduação
Programa de Pós-Graduação em Biotecnologia Industrial
UP
publisher.none.fl_str_mv Universidade Positivo
Brasil
Pós-Graduação
Programa de Pós-Graduação em Biotecnologia Industrial
UP
dc.source.none.fl_str_mv reponame:Repositório do Centro Universitário Braz Cubas
instname:Centro Universitário Braz Cubas (CUB)
instacron:CUB
instname_str Centro Universitário Braz Cubas (CUB)
instacron_str CUB
institution CUB
reponame_str Repositório do Centro Universitário Braz Cubas
collection Repositório do Centro Universitário Braz Cubas
repository.name.fl_str_mv Repositório do Centro Universitário Braz Cubas - Centro Universitário Braz Cubas (CUB)
repository.mail.fl_str_mv bibli@brazcubas.edu.br
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