Table 3.

Summary of in vitro studies on eye and AST.

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]