Lactoferrin Alleviates Acute Alcoholic Liver Injury by Improving Redox-Stress Response Capacity in Female C57BL/6J Mice

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.

Automated summary

The research shows that lactoferrin can attenuate acute alcoholic liver injury in female mice, with high-dose lactoferrin having significant alleviating effects. Lactoferrin pretreatment does not affect hepatic alcohol metabolism or reactive oxygen species levels induced by ethanol, suggesting a potential role of redox-stress response capacity in its effects. Lactoferrin may prevent acute ALI in female mice through promoting AKT and AMP-activated protein kinase activations and upregulating Nrf2 and LC3-II expressions.