Saffron and glaucoma. Effects of active components of an old natural neuroprotector

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 but controlling this pressure does not always prevent glaucomatous damage, so other harmful factors would be implicated in this pathologic process. Several mechanisms have been proposed that leads to the RGC death in glaucoma, including glutamate excitotoxicity, aggregation of misfolded proteins, mitochondrial dysfunction, oxidative stress, neurotrophic deprivation, and neuroinflammation, among others. Therefore, early diagnosis of neurodegeneration, understanding of its pathogenic mechanisms, and the development of new neuroprotective therapies represent major challenges for treating this disease.During the inflammatory process that occurs in glaucoma, retinal glial cells, both microglia and macroglia (Müller cells and astrocytes), become activated and release factors that can be neuroprotective in some cases and neurodegenerative in others. Cytokine‐ and chemokine‐mediated signalling engages in the neuroinflammatory process that leads to retinal ganglion cell (RGC) damage in glaucoma. Thus, a substance with anti‐inflammatory activity may protect against RGC degeneration.Increasing evidence from both experimental models and clinical studies in patients supports the neuroprotective effect of saffron components in neurodegenerative conditions and in retinal neurodegenerative pathologies, due to its important anti‐inflammatory, anti‐apoptotic, and antioxidant properties.This talk overviews the published studies that analysed the neuroprotective and anti‐inflammatory effects of saffron and its main components in both clinical trials and experimental models of glaucoma. All findings indicate that oral administration of saffron extract could be beneficial in glaucoma by decreasing the neuroinflammation associated with increased intraocular pressure, reducing microglial activation, regulating the production of proinflammatory cytokines, and preventing retinal ganglion cell death.