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Curcumin and Curcuminoids for Glaucoma NeuroprotectionGlaucoma is an age-related optic neuropathy marked by progressive retinal ganglion cell (RGC) loss and vision impairment. Chronic inflammation and oxidative stress are central to glaucomatous damage, suggesting anti-inflammatory antioxidants as neuroprotectants. Curcumin (the major curcuminoid from turmeric) has potent anti-inflammatory and antioxidant properties. It inhibits NF-κB (a pro-inflammatory transcription factor) and can activate Nrf2 (a master antioxidant regulator) () . These pleiotropic effects make curcumin a candidate for optic nerve protection. In the eye, microglia (resident immune cells) amplify inflammation when activated. Curcumin dampens microglial over-activation and cytokine release. In high-pressure glaucoma models, curcumin improved microglial survival and reduced oxidative damage (). In a retinal degeneration model (rd1 mice), curcumin suppressed microglial activation and chemokine secretion, decreasing apoptotic photoreceptors and improving function (). Thus, by modulating NF-κB, Nrf2, and microglial pathways, curcumin blunts the neuroinflammatory cascade in optic neuropathies () () ().Mechanisms: NF-κB, Nrf2, and MicrogliaNF-κB inhibition: In models of glaucoma-related stress (e.g. oxidative insult to trabecular meshwork), curcumin dramatically reduced inflammatory markers. For example, curcumin (20 µM) nearly abolished H₂O₂-induced increases in NF-κB–driven cytokines IL-6, IL-1α, IL-8 and adhesion molecule ELAM-1 in trabecular cells (). This demonstrates curcumin’s ability to suppress NF-κB–mediated inflammation in ocular cells. Other studies corroborate that curcumin reduces proinflammatory mediators (e.g. TNF-α, IL-1β) in diverse neural tissues by NF-κB blockade ().Nrf2 activation: Curcumin also boosts the antioxidant response. In oxidative stress models of the trabecular meshwork, curcumin activated the Nrf2/Keap1 pathway (), upregulating downstream antioxidant defenses. While specific ocular Nrf2 data are limited, curcumin is well-known to elevate Nrf2 and cytoprotective enzymes in CNS models. By tilting the balance toward antioxidation, curcumin helps neutralize reactive oxygen species that drive glaucomatous damage.Microglial modulation: Microglia-mediated inflammation is a key feature of optic neuropathy. Curcumin calms microglia through multiple mechanisms. In vitro, curcumin prevented oxidative stress–induced death of BV-2 microglia and reduced induction of caspase-3 and cytochrome c (). In a rat glaucoma model (chronic ocular hypertension), curcumin treatment preserved microglial viability, suggesting it counteracts glaucomatous oxidative injury to retinal glia (). In vivo, curcumin attenuated microglial activation and migration in degenerating retina: a study in rd1 mice showed significantly fewer amoeboid (activated) microglia after curcumin treatment, with concomitant reduction in chemokines and MMP-9 () (). Together, these findings indicate curcumin suppresses glial inflammation, stabilizing the retinal microenvironment.Neuroprotective Effects in Optic Neuropathy ModelsPreclinical models of glaucoma and optic nerve injury demonstrate curcumin’s neuroprotection. In an ex vivo optic nerve–cut model, eyeballs incubated for 24 hours exhibited marked RGC layer thinning and apoptosis. Curcumin pre-treatment prevented these changes: apoptotic caspases (Caspase-3/9) and stress kinases (p-JNK, p-ERK) did not rise, and RGC