crocin and Glaucoma

Crocin is a natural ingredient of saffron (Crocus sativus L.) flower that has shown potential for application as a supplement in eye health and preserving vision. Crocin has been examined for its potential to treat various eye diseases such as glaucoma, macular dystrophies, diabetic retinopathy, and age-related macular degeneration. This review briefly discusses the role of crocin in different eye diseases. The underlying pathophysiological pathways involved in the effect of crocin on ophthalmic diseases are also reviewed. Preclinical evidence shows the cytoprotective, antioxidative, anti-inflammatory, and blood-flow enhancing effects of crocin in retinal tissue. Crocin also affects the retinal pathologies by activating PI3K/Akt and inhibiting NF-κB signalling pathways. Clinical evidence suggests that crocin improves outcomes in patients with retinal degenerations, retinal dystrophies, and glaucoma. Overall, crocin can be suggested as a potential vision supplement in healthy populations and patients with eye diseases. However, more clinical studies with larger sample sizes and longer follow-up durations are needed to confirm the current evidence.

Topics: Antioxidants; Carotenoids; Glaucoma; Humans; Macular Degeneration; Phosphatidylinositol 3-Kinases; Plant Extracts

Glaucoma is a degenerative nerve disorder that results in irreversible blindness. It has been reported that the apoptosis of retinal ganglion cells (RGCs) is a hallmark of glaucoma. Oxidative stress is one of the major factors that cause apoptosis of RGCs. Crocin has many beneficial effects, including antioxidant and anti-apoptotic actions. However, the mechanism by which crocin protects against oxidative stress‑induced damage to RGCs remains unclear. The present study aimed to investigate the mechanism by which crocin protects RGC-5 cells against H2O2-induced damage. H2O2 was used to establish a model of oxidative stress injury in RGC-5 cells to mimic the development of glaucoma in vitro. Different concentrations (0.1 and 1 µM) of crocin were added to test whether crocin was capable of protecting RGCs from H2O2-induced damage. WST-1, lactic dehydrogenase (LDH) release and Annexin V/FITC assays were then performed. Levels of reactive oxygen species (ROS) were detected using a ROS assay kit, mitochondrial membrane potential (ΔΨm) was analyzed by JC-1 staining, caspase-3 activity was examined using a Caspase-3 assay kit, and the protein levels of Bax, Bcl-1 and cytochrome c were measured using western blot analysis. In addition, the protein level of phosphorylated nuclear factor-κB (p-NF-κB) p65 was also evaluated using western blot analysis. The results showed that crocin protected RGC-5 cells from apoptosis, decreased LDH release and enhanced cell viability. Additional experiments demonstrated that crocin decreased ROS levels, increased ΔΨm, downregulated the protein expression of Bax and cytochrome c, promoted Bcl-2 protein expression and activated NF-κB. Taken together, the findings of this study indicate that crocin prevented H2O2‑induced damage to RGCs through the mitochondrial pathway and activation of NF-κB.

Topics: Animals; Antioxidants; Apoptosis; Carotenoids; Cell Line; Cell Survival; Glaucoma; Humans; Hydrogen Peroxide; Membrane Potential, Mitochondrial; Mitochondria; NF-kappa B; Oxidative Stress; Phosphorylation; Protective Agents; Rats; Reactive Oxygen Species; Retinal Ganglion Cells; Signal Transduction