2 '-Fucosyllactose Ameliorates Oxidative Stress Damage in d-Galactose-Induced Aging Mice by Regulating Gut Microbiota and AMPK/SIRT1/FOXO1 Pathway

The imbalance of reactive oxygen species is the main cause in aging, accompanied by oxidative stress. As the most abundant in human milk oligosaccharides (HMOs), 2 & PRIME;-Fucosyllactose (2 & PRIME;-FL) has been confirmed to have great properties in immunity regulation and anti-inflammatory. The research on 2 & PRIME;-FL is focused on infants currently, while there is no related report of 2 & PRIME;-FL for the elderly. A d-galactose-induced accelerated aging model was established to explore the protective effect of 2 & PRIME;-FL on the intestines and brain in mice. In this study, 2 & PRIME;-FL significantly reduced oxidative stress damage and inflammation in the intestines of aging mice, potentially by regulating the sirtuin1 (SIRT1)-related and nuclear factor E2-related factor 2 (Nrf2) pathways. In addition, 2 & PRIME;-FL significantly improved the gut mucosal barrier function and increased the content of short-chain fatty acids (SCFAs) in the intestine. The gut microbiota analysis indicated that 2 & PRIME;-FL mainly increased the abundance of probiotics like Akkermansia in aging mice. Moreover, 2 & PRIME;-FL significantly inhibited apoptosis in the brains of aging mice, also increasing the expression of SIRT1. These findings provided a basis for learning the benefits of 2 & PRIME;-FL in the aging process.