Study2016Open access

Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma

Madeira MH, Ortin-Martinez A, Nadal-Nícolas F, Ambrósio AF, Vidal-Sanz M, Agudo-Barriuso M, Santiago AR

Scientific reports · 58 citations

How it was studied

Design
Animal study (classified by our AI screen)
Studied in
Animals
Main outcome
Health markers and function

Who paid for it

Funding
Independent funding
Government
Ministerio de Economía y Competitividad
Government
Fundação para a Ciência e a Tecnologia
Government
Instituto de Salud Carlos III
Grants
Fundação para a Ciência e a Tecnologia (04539); Fundação para a Ciência e a Tecnologia (COMPETE); Fundação para a Ciência e a Tecnologia (PTDC/BIM-MEC/0913/2012); Instituto de Salud Carlos III (RD 12/0034); Instituto de Salud Carlos III (PI13/00643); Fundação para a Ciência e a Tecnologia (UID/NEU/04539/2013); Instituto de Salud Carlos III (RD12/0034/0014); Ministerio de Economía y Competitividad (RD12/0034); Ministerio de Economía y Competitividad (PI13/00643); Fundação para a Ciência e a Tecnologia (FCOMP-01-0124-FEDER); Ministerio de Economía y Competitividad (RD12/0034/0014)

Based on 3 listed funder(s) and full-text disclosure statement.

Publication

Published
2016-06-08 · Sci Rep · vol. 6 · issue 1 · p. 27532
Publisher
Nature Portfolio
Cited
69 citations · more than 97% of similar papers · 6.4× the field average
Impact
Top 10% most cited in its field
References
68 works
Access
Open access (journal) · CC-BY
Research areas
Retinal Diseases and Treatments · Glaucoma and retinal disorders · Ocular Surface and Contact Lens
Keywords
Glaucoma, Medicine, Caffeine, Neuroinflammation, Retinal ganglion cell, Retinal, Neuroprotection, Ocular hypertension, Intraocular pressure, Pharmacology, Intravitreal administration, Optic nerve, Adenosine receptor antagonist, Retina, Ophthalmology, Neuroscience, Adenosine receptor, Receptor, Endocrinology, Internal medicine, Biology, Inflammation
MeSH
central nervous system, retinal ganglion cells, retina, animals, humans, rats, rats, sprague-dawley, glaucoma, disease models, animal, inflammation, nerve degeneration, caffeine, intraocular pressure

7 authors

From PT, ES

  • Maria Helena MadeiraUniversity of Coimbra
  • Arturo Ortín-MartínezInstituto Murciano de Investigación Biosanitaria; Universidad de Murcia
  • Francisco Manuel Nadal-NicolásInstituto Murciano de Investigación Biosanitaria; Universidad de Murcia
  • António Francisco AmbrósioAssociation for Innovation and Biomedical Research on Light and Image; University of Coimbra
  • Manuel Vidal‐SanzInstituto Murciano de Investigación Biosanitaria; Universidad de Murcia
  • Marta Agudo‐BarriusoInstituto Murciano de Investigación Biosanitaria; Universidad de Murcia

Abstract

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.

Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).

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