Caffeine Protects Against Retinal Inflammation

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Abstract

Caffeine, one of the most consumed central nervous system (CNS) stimulants, is an antagonist of A ₁ and A _2A adenosine receptors. In this study, we investigated the potential protective effects of this methylxanthine in the retinal tissue. We tested caffeine by using in vitro and in vivo paradigms of retinal inflammation. Human retinal pigment epithelial cells (ARPE-19) were exposed to lipopolysaccharide (LPS) with or without caffeine. This latter was able to reduce the inflammatory response in ARPE-19 cells exposed to LPS, attenuating the release of IL-1β, IL-6, and TNF-α and the nuclear translocation of p-NFκB. Additionally, caffeine treatment restored the integrity of the ARPE-19 monolayer assessed by transepithelial electrical resistance (TEER) and the sodium fluorescein permeability test. Finally, the ischemia reperfusion (I/R) injury model was used in C57BL/6J mice to induce retinal inflammation and investigate the effects of caffeine treatment. Mouse eyes were treated topically with caffeine, and a pattern electroretinogram (PERG) was used to assess the retinal ganglion cell (RGC) function; furthermore, we evaluated the levels of IL-6 and BDNF in the retina. Retinal BDNF dropped significantly ( p < 0.05) in the I/R group compared to the control group (normal mice); on the contrary, caffeine treatment maintained physiological levels of BDNF in the retina of I/R eyes. Caffeine was also able to reduce IL-6 mRNA levels in the retina of I/R eyes. In conclusion, these findings suggest that caffeine is a good candidate to counteract inflammation in retinal diseases.

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International Union of Basic and Clinical Pharmacology. LXXXI. Nomenclature and classification of adenosine receptors--an update.

Bertil Fredholm, Adriaan P IJzerman, Kenneth A. Jacobson … (2011)

In the 10 years since our previous International Union of Basic and Clinical Pharmacology report on the nomenclature and classification of adenosine receptors, no developments have led to major changes in the recommendations. However, there have been so many other developments that an update is needed. The fact that the structure of one of the adenosine receptors has recently been solved has already led to new ways of in silico screening of ligands. The evidence that adenosine receptors can form homo- and heteromultimers has accumulated, but the functional significance of such complexes remains unclear. The availability of mice with genetic modification of all the adenosine receptors has led to a clarification of the functional roles of adenosine, and to excellent means to study the specificity of drugs. There are also interesting associations between disease and structural variants in one or more of the adenosine receptors. Several new selective agonists and antagonists have become available. They provide improved possibilities for receptor classification. There are also developments hinting at the usefulness of allosteric modulators. Many drugs targeting adenosine receptors are in clinical trials, but the established therapeutic use is still very limited.

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Retinal ischemia: mechanisms of damage and potential therapeutic strategies.

Neville N. Osborne, Robert J. Casson, John Wood … (2004)

Retinal ischemia is a common cause of visual impairment and blindness. At the cellular level, ischemic retinal injury consists of a self-reinforcing destructive cascade involving neuronal depolarisation, calcium influx and oxidative stress initiated by energy failure and increased glutamatergic stimulation. There is a cell-specific sensitivity to ischemic injury which may reflect variability in the balance of excitatory and inhibitory neurotransmitter receptors on a given cell. A number of animal models and analytical techniques have been used to study retinal ischemia, and an increasing number of treatments have been shown to interrupt the "ischemic cascade" and attenuate the detrimental effects of retinal ischemia. Thus far, however, success in the laboratory has not been translated to the clinic. Difficulties with the route of administration, dosage, and adverse effects may render certain experimental treatments clinically unusable. Furthermore, neuroprotection-based treatment strategies for stroke have so far been disappointing. However, compared to the brain, the retina exhibits a remarkable natural resistance to ischemic injury, which may reflect its peculiar metabolism and unique environment. Given the increasing understanding of the events involved in ischemic neuronal injury it is hoped that clinically effective treatments for retinal ischemia will soon be available.

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Inflammation in diabetic retinopathy.

Johannes Kern, Johnny Tang (2011)

Diabetes causes a number of metabolic and physiologic abnormalities in the retina, but which of these abnormalities contribute to recognized features of diabetic retinopathy (DR) is less clear. Many of the molecular and physiologic abnormalities that have been found to develop in the retina in diabetes are consistent with inflammation. Moreover, a number of anti-inflammatory therapies have been found to significantly inhibit development of different aspects of DR in animal models. Herein, we review the inflammatory mediators and their relationship to early and late DR, and discuss the potential of anti-inflammatory approaches to inhibit development of different stages of the retinopathy. We focus primarily on information derived from in vivo studies, supplementing with information from in vitro studies were important. Copyright © 2011 Elsevier Ltd. All rights reserved.

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Author and article information

Contributors

Federica Conti: URI : https://loop.frontiersin.org/people/1388120/overview

Francesca Lazzara: URI : https://loop.frontiersin.org/people/1205738/overview

Giovanni Luca Romano: URI : https://loop.frontiersin.org/people/1346311/overview

Chiara Bianca Maria Platania: URI : https://loop.frontiersin.org/people/196066/overview

Filippo Drago: URI : https://loop.frontiersin.org/people/16703/overview

Claudio Bucolo: URI : https://loop.frontiersin.org/people/22151/overview

Journal

Journal ID (nlm-ta): Front Pharmacol

Journal ID (iso-abbrev): Front Pharmacol

Journal ID (publisher-id): Front. Pharmacol.

Title: Frontiers in Pharmacology

Publisher: Frontiers Media S.A.

ISSN (Electronic): 1663-9812

Publication date (Electronic): 06 January 2022

Publication date Collection: 2021

Volume: 12

Electronic Location Identifier: 824885

Affiliations

[1] ¹ Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania , Catania, Italy

[2] ² Center for Research in Ocular Pharmacology-CERFO, University of Catania , Catania, Italy

Author notes

Edited by: Cesare Mancuso, Catholic University of the Sacred Heart, Italy

Reviewed by: Jennifer Arcuri, University of Miami Health System, United States

Monica Baiula, University of Bologna, Italy

*Correspondence: Claudio Bucolo, claudio.bucolo@ 123456unict.it

[ † ]

These authors have contributed equally to this work

This article was submitted to Experimental Pharmacology and Drug Discovery, a section of the journal Frontiers in Pharmacology

Article

Publisher ID: 824885

DOI: 10.3389/fphar.2021.824885

PMC ID: 8773454

PubMed ID: 35069225

SO-VID: 8d224852-a5f6-472b-a890-40a3c4051298

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This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

History

Date received : 29 November 2021

Date accepted : 13 December 2021

Funding

Funded by: Università di Catania , doi 10.13039/501100004505;

Funded by: Ministero Dell’Istruzione, dell’Università e Della Ricerca , doi 10.13039/501100003407;

Caffeine Protects Against Retinal Inflammation

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Most cited references 90

International Union of Basic and Clinical Pharmacology. LXXXI. Nomenclature and classification of adenosine receptors--an update.

Retinal ischemia: mechanisms of damage and potential therapeutic strategies.

Inflammation in diabetic retinopathy.

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