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

• Published in: Scientific reports 2016-06, Vol.6 (1), p.27532-27532, Article 27532
• Main Authors: Madeira, Maria H., Ortin-Martinez, Arturo, Nadal-Nícolas, Francisco, Ambrósio, António F., Vidal-Sanz, Manuel, Agudo-Barriuso, Marta, Santiago, Ana Raquel
• Format: Article
• Language: English
• Subjects: 14/28; 692/308/1426; 692/699/3161/3169/3170; 82/51; 82/80; Adenosine; Animal models; Animals; Caffeine; Caffeine - administration & dosage; Central nervous system; Central Nervous System - drug effects; Central Nervous System - injuries; Disease Models, Animal; Drinking water; Glaucoma; Glaucoma - complications; Glaucoma - drug therapy; Glaucoma - physiopathology; Humanities and Social Sciences; Humans; Hypertension; Inflammation - complications; Inflammation - drug therapy; Inflammation - physiopathology; Intraocular Pressure - drug effects; multidisciplinary; Nerve Degeneration - complications; Nerve Degeneration - drug therapy; Nerve Degeneration - physiopathology; Proteins; Rats; Rats, Sprague-Dawley; Retina - drug effects; Retina - physiopathology; Retinal Ganglion Cells - drug effects; Retinal Ganglion Cells - pathology; Risk factors; Science; Tumor necrosis factor-TNF
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/srep27532

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.