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　mu　M)　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　(Delta　Psi　m)　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-kappa　B　(p-NF-kappa　B)　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　Delta　Psi　m,　downregulated　the　protein　expression　of　Bax　and　cytochrome　c,　promoted　Bcl-2　protein　expression　and　activated　NF-kappa　B.　Taken　together,　the　findings　of　this　study　indicate　that　crocin　prevented　H2O2-induced　damage　to　RGCs　through　the　mitochondrial　pathway　and　activation　of　NF-kappa　B.