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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.
Highlights
Cultures[15] as well as in the high intraocular pressure (IOP)-induced transient ischemic injury animal model[16]
Ocular hypertension induced by laser photocoagulation (LP) of the limbal and episcleral vessels of adult rats triggers anatomical and functional alterations associated with glaucoma, such as loss of retinal ganglion cells (RGCs) and impaired retrograde axonal transport of the optic nerve[24,25]
By quantitative PCR (qPCR), we evaluated the mRNA levels of two markers of microglia reactivity, major histocompatibility complex class II (MHC-II) (Fig. 4A) and translocator protein (18 kDa) (TSPO)[32,33,34] (Fig. 4B), as well as CD11b, a general marker of microglia (Fig. 4C) and triggering receptor expressed on myeloid cells 2 (TREM2), which is associated with microglia phagocytic capacity (Fig. 4D)
Summary
Cultures[15] as well as in the high IOP-induced transient ischemic injury animal model[16]. The main aim of this work was to investigate whether caffeine administration modulates retinal neuroinflammation and prevents the loss of RGCs in an animal model (Sprague Dawley rats) of ocular hypertension (OHT), obtained by laser photocoagulation (LP) of the trabecular meshwork and limbal veins. This model does not completely mimic human glaucomatous optic neuropathy, it has been extensively used to evaluate anatomical and functional alterations associated with glaucomatous damage, such as loss of RGCs and impairment of the retrograde axonal transport in the optic nerve[24,25,26,27]
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