Imunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxina

Detalhes bibliográficos
Autor(a) principal: Gomes, Henrique Mautone
Data de Publicação: 2019
Tipo de documento: Trabalho de conclusão de curso
Idioma: por
Título da fonte: Repositório Institucional da UFRGS
Texto Completo: http://hdl.handle.net/10183/237552
Resumo: The receptor for advanced glycation end products (RAGE) is a multiligand membrane receptor associated with a variety of roles depending on the tissue evaluated and its activation is believed to sustain a proinflammatory state in the system. Also, it has been shown that blockage of RAGE can somehow display a protective effect against insults induced by Lipopolysaccharide (LPS) endotoxemia. LPS is widely used to mimic strong and acute inflammation in mammals and also as a model for Endotoxin Induced Uveitis (EIU) in rodents. Materials and Methods: In this work we evaluated if pre-treatment with anti-RAGE IgG could have a protective effect in the retinas of Wistar Rats. Animals (60 days old) were randomly distributed into 2 treated groups and 2 control groups and had their retinas collected 24 hours after induction of EIU via LPS endotoxemia. Catalase activity and also the levels of protein and lipid oxidation were used as oxidative stress markers and some RAGE downstream signaling molecules were quantified by western blotting. Results: We observed that RAGE blockage associated with LPS reduced the phosphorylation of ERK1/2, Stat3 and P65 and increased Catalase activity while not altering oxidative damage markers. Conclusion: Our results indicate us that RAGE has a pivotal role in retinal tissue mainly mediating signal transducing factors. Oxidative damage markers were not elevated in retinal tissue however this may be a time-dependent issue since we used a short-term protocol for evaluating LPS endotoxemia and phosphorylation of NFKB ligands was observed.
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spelling Gomes, Henrique MautoneMoreira, Jose Claudio FonsecaGasparotto, Juciano2022-04-20T04:50:28Z2019http://hdl.handle.net/10183/237552001128435The receptor for advanced glycation end products (RAGE) is a multiligand membrane receptor associated with a variety of roles depending on the tissue evaluated and its activation is believed to sustain a proinflammatory state in the system. Also, it has been shown that blockage of RAGE can somehow display a protective effect against insults induced by Lipopolysaccharide (LPS) endotoxemia. LPS is widely used to mimic strong and acute inflammation in mammals and also as a model for Endotoxin Induced Uveitis (EIU) in rodents. Materials and Methods: In this work we evaluated if pre-treatment with anti-RAGE IgG could have a protective effect in the retinas of Wistar Rats. Animals (60 days old) were randomly distributed into 2 treated groups and 2 control groups and had their retinas collected 24 hours after induction of EIU via LPS endotoxemia. Catalase activity and also the levels of protein and lipid oxidation were used as oxidative stress markers and some RAGE downstream signaling molecules were quantified by western blotting. Results: We observed that RAGE blockage associated with LPS reduced the phosphorylation of ERK1/2, Stat3 and P65 and increased Catalase activity while not altering oxidative damage markers. Conclusion: Our results indicate us that RAGE has a pivotal role in retinal tissue mainly mediating signal transducing factors. Oxidative damage markers were not elevated in retinal tissue however this may be a time-dependent issue since we used a short-term protocol for evaluating LPS endotoxemia and phosphorylation of NFKB ligands was observed.application/pdfporEndotoxin Induced UveitisAnti-RAGE IgGRetinal tissueCatalase activityNFKB signalingImunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxinainfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/bachelorThesisUniversidade Federal do Rio Grande do SulInstituto de BiociênciasPorto Alegre, BR-RS2019Ciências Biológicas: Bachareladograduaçãoinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001128435.pdf.txt001128435.pdf.txtExtracted Texttext/plain48306http://www.lume.ufrgs.br/bitstream/10183/237552/2/001128435.pdf.txt0955490c1ba44192db51fda82671abe8MD52ORIGINAL001128435.pdfTexto completoapplication/pdf1134579http://www.lume.ufrgs.br/bitstream/10183/237552/1/001128435.pdffd41d6bd1cc3f1ac1ff0a80f631ff31dMD5110183/2375522022-04-28 04:42:36.976985oai:www.lume.ufrgs.br:10183/237552Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2022-04-28T07:42:36Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false
dc.title.pt_BR.fl_str_mv Imunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxina
title Imunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxina
spellingShingle Imunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxina
Gomes, Henrique Mautone
Endotoxin Induced Uveitis
Anti-RAGE IgG
Retinal tissue
Catalase activity
NFKB signaling
title_short Imunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxina
title_full Imunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxina
title_fullStr Imunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxina
title_full_unstemmed Imunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxina
title_sort Imunobloqueio de RAGE reduz a sinalização de NFkB e aumenta a atividade de catalase na retina após Uveíte induzida por Endotoxina
author Gomes, Henrique Mautone
author_facet Gomes, Henrique Mautone
author_role author
dc.contributor.author.fl_str_mv Gomes, Henrique Mautone
dc.contributor.advisor1.fl_str_mv Moreira, Jose Claudio Fonseca
Gasparotto, Juciano
contributor_str_mv Moreira, Jose Claudio Fonseca
Gasparotto, Juciano
dc.subject.eng.fl_str_mv Endotoxin Induced Uveitis
Anti-RAGE IgG
Retinal tissue
Catalase activity
NFKB signaling
topic Endotoxin Induced Uveitis
Anti-RAGE IgG
Retinal tissue
Catalase activity
NFKB signaling
description The receptor for advanced glycation end products (RAGE) is a multiligand membrane receptor associated with a variety of roles depending on the tissue evaluated and its activation is believed to sustain a proinflammatory state in the system. Also, it has been shown that blockage of RAGE can somehow display a protective effect against insults induced by Lipopolysaccharide (LPS) endotoxemia. LPS is widely used to mimic strong and acute inflammation in mammals and also as a model for Endotoxin Induced Uveitis (EIU) in rodents. Materials and Methods: In this work we evaluated if pre-treatment with anti-RAGE IgG could have a protective effect in the retinas of Wistar Rats. Animals (60 days old) were randomly distributed into 2 treated groups and 2 control groups and had their retinas collected 24 hours after induction of EIU via LPS endotoxemia. Catalase activity and also the levels of protein and lipid oxidation were used as oxidative stress markers and some RAGE downstream signaling molecules were quantified by western blotting. Results: We observed that RAGE blockage associated with LPS reduced the phosphorylation of ERK1/2, Stat3 and P65 and increased Catalase activity while not altering oxidative damage markers. Conclusion: Our results indicate us that RAGE has a pivotal role in retinal tissue mainly mediating signal transducing factors. Oxidative damage markers were not elevated in retinal tissue however this may be a time-dependent issue since we used a short-term protocol for evaluating LPS endotoxemia and phosphorylation of NFKB ligands was observed.
publishDate 2019
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