Abstract
Lactoferrin (Lf) can attenuate alcoholic liver injury (ALI) in male mice; however, the effects of Lf on acute ALI in female mice are still unknown. Female C57BL/6J mice were randomly divided into four groups and fed with different diets for 4 weeks: an AIN-93G diet for control (CON) and ethanol (EtOH) groups; an AIN-93G diet with 0.4 and 4% casein replaced by Lf for low-dose Lf (LLf) and high-dose Lf (HLf) groups. Acute ALI was induced by intragastric administration of ethanol (4.8 g/kgbw) every 12 h continuously for three times. HLf had obvious alleviating effects on acute ALI. Lf pretreatment did not affect hepatic alcohol metabolism key enzymes. Meanwhile, the ethanol-induced hepatic reactive oxygen species level increase was not ameliorated by Lf. Metabolomics and bioinformatics analysis results suggested an important role of redox-stress response capacity (RRC). Western blots showed HLf-promoted AKT and AMP-activated protein kinase activations and upregulated Nrf2 and LC3-II expressions, which was associated with RRC improvement. In summary, HLf could prevent acute ALI in female mice, and RRC likely played an important role.