Egg yolk lecithin alleviates fatigue in flood-stressed mice by modulating hypothalamic microglial activation and the hepatic AKT/GSK3β pathway to attenuate neuroinflammation and metabolic dysregulation.

Given its known anti-inflammatory and cognitive-enhancing properties, egg yolk lecithin (EYL) shows therapeutic potential for mitigating fatigue in flood-confined mice. EYL supplementation alleviated key pathological manifestations of flood confinement in mice, including body composition loss, metabolic waste accumulation, neuroinflammation, and motor deficits. Mechanistically, EYL supplementation suppressed the excessive activation of microglia, which led to a reduction in the expression of TNF-α and IL-1β in the brain. Additionally, it partially restored the homeostasis of neurotransmitter and hormone metabolism within the HPA axis. Furthermore, EYL facilitated the phosphorylation of the AKT/GSK3β pathway, thereby maintaining energy metabolic homeostasis. Reduction of neuroinflammatory-promoting metabolites like blood ammonia and urea nitrogen, achieved through maintained metabolic homeostasis, alleviated neuroinflammation. Moreover, it also preserved motor function by sustaining muscular energy supply and suppressing Caspase-9 dependent apoptosis. These results position EYL as a promising candidate for emergency foods to enhance survival outcomes in disasters.