Objective        To observe the effect of alcohol exposure on the retina of neonatal mice and the neuroprotective role of liver X receptor (LXR) agonist TO901317 (TO).       Methods        Mice were randomly divided into 3 groups

including a control group

an alcohol exposure group and a TO pretreatment group (n=3). Hematoxylin and eosin (HE) staining was used to observe the general structure of mouse retina

and immunochemistry was applied to detect NeuN-positive neurons and GFAP expression in the retina.       Results        LXRβ was mainly expressed in retinal ganglion cell layer of neonatal (postnatal day 6

P6) mice. HE staining showed a significant decrease in cell number in retinal ganglion cell layer of the alcohol exposure group compared with the control group (P0.01)

while TO could protect the ganglion cells from alcohol damage (P0.05). Compared with the control group

NeuN-positive cells in the retinal ganglion cell layer of the alcohol exposure group significantly decreased (P0.01)

but the TO pretreatment group had more NeuN-positive cells than the alcohol exposure group (P0.01). GFAP expression significantly increased in the retinal ganglion cell layer of the alcohol exposure group as compared with the control group and TO pretreatment group (P0.01).       Conclusion        LXR agonist TO can inhibit alcohol-induced astrocyte activation in retina and rescue retinal ganglion cells in neonatal mice.