Abstract
Glaucoma is a neurodegenerative disease characterized by the loss of retinal ganglion cells (RGCs). An increase in the intraocular pressure is the principal risk factor for such loss, but controlling this pressure does not always prevent glaucomatous damage. Activation of immune cells resident in the retina (microglia) may contribute to RGC death. Thus, a substance with anti-inflammatory activity may protect against RGC degeneration. This study investigated the neuroprotective and anti-inflammatory effects of a hydrophilic saffron extract standardized to 3% crocin content in a mouse model of unilateral, laser-induced ocular hypertension (OHT). Treatment with saffron extract decreased microglion numbers and morphological signs of their activation, including soma size and process retraction, both in OHT and in contralateral eyes. Saffron extract treatment also partially reversed OHT-induced down-regulation of P2RY12. In addition, the extract prevented retinal ganglion cell death in OHT eyes. Oral administration of saffron extract was able to decrease the neuroinflammation associated with increased intraocular pressure, preventing retinal ganglion cell death. Our findings indicate that saffron extract may exert a protective effect in glaucomatous pathology.
Highlights
Glaucoma is one of the leading causes of irreversible blindness in the world
We used a mouse model of unilateral, laser-induced ocular hypertension (OHT) to study the possible protective effects of saffron extract in glaucomatous neuropathy. This is one of the experimental models available to study the mechanism by which Intraocular pressure (IOP) can cause retinal damage, and this model could be useful for testing neuroprotective substances to prevent ganglion cell death [3]
Laser-induced OHT, a substantial increase in IOP was evident on the first day after laser photocoagulation of the limbal and episcleral veins
Summary
Glaucoma is one of the leading causes of irreversible blindness in the world. It is characterized by retinal ganglion cell (RGC) death which leads to a progressive visual field loss and blindness [1]. To study RGC death in glaucoma, a variety of rat and mouse models have been used, including the use of hypertonic saline injection into the episcleral veins, cauterization or ligation of episcleral veins, or laser photocoagulation of the perilimbal region [3,4]. The studies performed in these models have proposed various mechanisms of RGC death in glaucoma, including glutamate excitotoxicity, aggregation of misfolded proteins, mitochondrial dysfunction, oxidative stress, neurotrophic deprivation, and neuroinflammation, among others [2,5,6,7]
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