| Study type | Cell lines | AST dose | Referred ocular disease | Biological effects | Related genes | References |
| In vitre | ARPE-19 | 0/5/10/20 μm | AMD | Attenuated H2O2-induced oxidative stress | NQO1, HO-1, GCLC, GCLM, Nrf2, PI3K, Akt, caspase 3 | [87] | Active Nrf2-ARE, PI3K/Akt pathway | In vitro | ARPE-19 | 50/150 μm | AMD | Inhibit inflammatory and angiogenic molecules and NF-κB activation | IL-6, VEGR-1, VEGR-2, MCP-1, ICAM-2, IκB, NF-κB, p65 | [15] | In vitro | 661W cells | 3/10/20 μm | AMD | Active Nrf2 | Nrf2, c-Jun, phaseII enzymes (HO-1, Mqo-1, GCLM) | [52] | Reduce ROS production | Mitigate photoreceptor cell death | In vitro | 661W cells | 0–50 μm | AMD | Reduce ROS production | Bcl-2, Bax, PI3K, Akt, ROS phaseII enzymes (HO-1, NQO1) | [83] | Inhibit cell death, oxidative stress markers, phaseII enzymes expression and Nrf2/PI3K/Akt pathway | In vitro | RGC-5 | 0.01/0.1/1/10 μm | Glaucoma | Reduce cell death and ROS production | — | [58] | In vitro | RGC-5 | 1/10/100 nm | Glaucoma | Increase survival rate of cell death induced by glutamate/oxidative stress/hypoxia | — | [84] | Inhibit DNA oxidative damage, apoptosis and necrotic RGCs death | In vitro | RGC-5 | 0.1–10 μm | Retinal ischemia reperfusion | Reduced ROS production | — | [53] | In vitro | HCECs | 0.2/1/2/10 μm | Phototoxic keratitis | Increase cell viability | ROS, p53, p32, p16 | [85] | Reduced ROS production and age-related factors | In vitro | HCECs TKE2 cells | 1/0.1/0.01 mg/ml | Phototoxic keratitis | Decrease cytotoxicity | 8-OHdG | [44] | In vitro | HLECs SRA 01–04 | 1/2/4 μm | cataract | Inhibit UV-induced oxidative stress activity and lipid peroxidation | p-JNK, p38 | [86] |
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