Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma
Autor(a) principal: | |
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Data de Publicação: | 2016 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10316/108906 https://doi.org/10.1038/srep27532 |
Resumo: | Glaucoma is the second leading cause of blindness worldwide, being characterized by progressive optic nerve damage and loss of retinal ganglion cells (RGCs), accompanied by increased inflammatory response involving retinal microglial cells. The etiology of glaucoma is still unknown, and despite elevated intraocular pressure (IOP) being a major risk factor, the exact mechanisms responsible for RGC degeneration remain unknown. Caffeine, which is an antagonist of adenosine receptors, is the most widely consumed psychoactive drug in the world. Several evidences suggest that caffeine can attenuate the neuroinflammatory responses and afford protection upon central nervous system (CNS) injury. We took advantage of a well characterized animal model of glaucoma to investigate whether caffeine administration controls neuroinflammation and elicits neuroprotection. Caffeine or water were administered ad libitum and ocular hypertension (OHT) was induced by laser photocoagulation of the limbal veins in Sprague Dawley rats. Herein, we show that caffeine is able to partially decrease the IOP in ocular hypertensive animals. More importantly, we found that drinking caffeine prevented retinal microglia-mediated neuroinflammatory response and attenuated the loss of RGCs in animals with ocular hypertension (OHT). This study opens the possibility that caffeine or adenosine receptor antagonists might be a therapeutic option to manage RGC loss in glaucoma. |
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Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucomaAnimalsCaffeineCentral Nervous SystemDisease Models, AnimalGlaucomaHumansInflammationIntraocular PressureNerve DegenerationRatsRats, Sprague-DawleyRetinaRetinal Ganglion CellsGlaucoma is the second leading cause of blindness worldwide, being characterized by progressive optic nerve damage and loss of retinal ganglion cells (RGCs), accompanied by increased inflammatory response involving retinal microglial cells. The etiology of glaucoma is still unknown, and despite elevated intraocular pressure (IOP) being a major risk factor, the exact mechanisms responsible for RGC degeneration remain unknown. Caffeine, which is an antagonist of adenosine receptors, is the most widely consumed psychoactive drug in the world. Several evidences suggest that caffeine can attenuate the neuroinflammatory responses and afford protection upon central nervous system (CNS) injury. We took advantage of a well characterized animal model of glaucoma to investigate whether caffeine administration controls neuroinflammation and elicits neuroprotection. Caffeine or water were administered ad libitum and ocular hypertension (OHT) was induced by laser photocoagulation of the limbal veins in Sprague Dawley rats. Herein, we show that caffeine is able to partially decrease the IOP in ocular hypertensive animals. More importantly, we found that drinking caffeine prevented retinal microglia-mediated neuroinflammatory response and attenuated the loss of RGCs in animals with ocular hypertension (OHT). This study opens the possibility that caffeine or adenosine receptor antagonists might be a therapeutic option to manage RGC loss in glaucoma.Springer Nature2016-06-08info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/108906http://hdl.handle.net/10316/108906https://doi.org/10.1038/srep27532eng2045-2322Madeira, Maria H.Ortin-Martinez, ArturoNadal-Nícolas, FranciscoAmbrósio, António F.Vidal-Sanz, ManuelAgudo-Barriuso, MartaSantiago, Ana Raquelinfo:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-09-25T07:44:36Zoai:estudogeral.uc.pt:10316/108906Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T21:25:08.617686Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma |
title |
Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma |
spellingShingle |
Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma Madeira, Maria H. Animals Caffeine Central Nervous System Disease Models, Animal Glaucoma Humans Inflammation Intraocular Pressure Nerve Degeneration Rats Rats, Sprague-Dawley Retina Retinal Ganglion Cells |
title_short |
Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma |
title_full |
Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma |
title_fullStr |
Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma |
title_full_unstemmed |
Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma |
title_sort |
Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma |
author |
Madeira, Maria H. |
author_facet |
Madeira, Maria H. Ortin-Martinez, Arturo Nadal-Nícolas, Francisco Ambrósio, António F. Vidal-Sanz, Manuel Agudo-Barriuso, Marta Santiago, Ana Raquel |
author_role |
author |
author2 |
Ortin-Martinez, Arturo Nadal-Nícolas, Francisco Ambrósio, António F. Vidal-Sanz, Manuel Agudo-Barriuso, Marta Santiago, Ana Raquel |
author2_role |
author author author author author author |
dc.contributor.author.fl_str_mv |
Madeira, Maria H. Ortin-Martinez, Arturo Nadal-Nícolas, Francisco Ambrósio, António F. Vidal-Sanz, Manuel Agudo-Barriuso, Marta Santiago, Ana Raquel |
dc.subject.por.fl_str_mv |
Animals Caffeine Central Nervous System Disease Models, Animal Glaucoma Humans Inflammation Intraocular Pressure Nerve Degeneration Rats Rats, Sprague-Dawley Retina Retinal Ganglion Cells |
topic |
Animals Caffeine Central Nervous System Disease Models, Animal Glaucoma Humans Inflammation Intraocular Pressure Nerve Degeneration Rats Rats, Sprague-Dawley Retina Retinal Ganglion Cells |
description |
Glaucoma is the second leading cause of blindness worldwide, being characterized by progressive optic nerve damage and loss of retinal ganglion cells (RGCs), accompanied by increased inflammatory response involving retinal microglial cells. The etiology of glaucoma is still unknown, and despite elevated intraocular pressure (IOP) being a major risk factor, the exact mechanisms responsible for RGC degeneration remain unknown. Caffeine, which is an antagonist of adenosine receptors, is the most widely consumed psychoactive drug in the world. Several evidences suggest that caffeine can attenuate the neuroinflammatory responses and afford protection upon central nervous system (CNS) injury. We took advantage of a well characterized animal model of glaucoma to investigate whether caffeine administration controls neuroinflammation and elicits neuroprotection. Caffeine or water were administered ad libitum and ocular hypertension (OHT) was induced by laser photocoagulation of the limbal veins in Sprague Dawley rats. Herein, we show that caffeine is able to partially decrease the IOP in ocular hypertensive animals. More importantly, we found that drinking caffeine prevented retinal microglia-mediated neuroinflammatory response and attenuated the loss of RGCs in animals with ocular hypertension (OHT). This study opens the possibility that caffeine or adenosine receptor antagonists might be a therapeutic option to manage RGC loss in glaucoma. |
publishDate |
2016 |
dc.date.none.fl_str_mv |
2016-06-08 |
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 |
http://hdl.handle.net/10316/108906 http://hdl.handle.net/10316/108906 https://doi.org/10.1038/srep27532 |
url |
http://hdl.handle.net/10316/108906 https://doi.org/10.1038/srep27532 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
2045-2322 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.publisher.none.fl_str_mv |
Springer Nature |
publisher.none.fl_str_mv |
Springer Nature |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
instacron_str |
RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
collection |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository.name.fl_str_mv |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
repository.mail.fl_str_mv |
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1799134134442917888 |