Objective       To determine the protective effect of ac

tivating endogenous liver X receptors (LXRs) on the proliferation of dentate gyrus (DG) neural precursor cells (NPCs) in the neonatal mice exposed to ethanol.       Methods        Mice from the same litters were randomized into a control group (equivalent solvent)

an ethanol group and an ethanol group pretreated with LXRs agonist TO901317  (10 mg/kg

dissolved in solvent DMSO∶PBS=1∶3) (TO + ethanol group). Immunohistochemistry assay was used to detect the expression of Ki67 protein (Ki67)

5-bromo-2′-deoxyuridine (BrdU)

sex determining region Y-box 2 (Sox2) and nestin to observe whether the activation of LXRs could promote the cell proliferation and maintain NPCs in the DG of the hippocampus of neonatal mice exposed to ethanol.       Results       The inhibited proliferation of NPCs in the hippocampus was proven by significant reduction in the number of Ki67-positive cells [ethanol group (24.7±5.5) vs control group (45.9±7.1)

P

0.01

]

BrdU-positive cells [ethanol group (44.9±2.9) vs control group (54.8±6.0)

P

0.01

]

and Sox2-labeled cells [ethanol group (31.1±6.4) vs control group (46.6±6.3)

P

0.01

]

in the neonatal mice subjected to ethanol exposure

which could be rescued by pretreatment of TO901317 [Ki67-positive cells: ethanol group (24.7±5.5) vs TO + ethanol group (54.2±10.8)

P

0.01; BrdU-positive cells: ethanol group (44.9±2.9) vs TO+ethanol group (53.4±2.8)

P

0.01; Sox2-labeled cells: ethanol group (31.1±6.4) vs TO+ethanol group (54.0±6.7)

P

0.01

]

. Meanwhile

TO901317 also rescued the number decrease of nestin-positive radial glial cell fibers caused by ethanol exposure [control group (35.0±2.0) vs ethanol group (25.3±3.8) vs TO+ethanol group (33.0±2.6)

P

0.01

]

.       Conclusion       Activation of LXRs can rescue the decline of NPCs proliferation in the DG of the hippocampus in ethanol-exposed neonatal mice.