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Western diet (rich in highly refined sugar and fat) can induce a range of metabolic dysfunctions in animals and humans, including neuroinflammation and cognitive function decline. Neuroinflammation and cognitive impairment, two critical pathological characteristics of Alzheimer’s disease, have been closely associated with microbial alteration via the gut-brain axis. Thus, the present study aimed to investigate the influence of 2-O-β-D-glucopyranosyl-L-ascorbic acid (AA-2βG) isolated from the fruits of Lycium barbarumon preventing the high-fructose diet (HFrD) induced neuroinflammation in mice. It was found that AA-2βG prevented HFrD-induced cognitive deficits. AA-2βG also predominantly enhanced the gut barrier integrity, decreased lipopolysaccharide entry into the circulation, which subsequently countered the activation of glial cells and neuroinflammatory response. These beneficial effects were transmissible by horizontal fecal microbiome transplantation, transferring from AA-2βG fed mice to HFrD fed mice. Additionally, AA-2βG exerted neuroprotective effects involving the enrichment of Lactobacillusand Akkermansia, potentially beneficial intestinal bacteria. The present study provided the evidence that AA-2βG could improve indices of cognition and neuroinflammmation via modulating gut dybiosis and preventing leaky gut. As a potential functional food ingredient, AA-2βG may be applied to attenuate neuroinflammation associated with Western-style diets.

β-Carotene, a typical non-oxygenated carotenoid, is the most efficient source of retinol (VA). The low bio-availability of β-carotene lead to large accumulation in colon; however, the relationship between β-carotene and gut microflora remains unclear. This study intends to explore the interaction between β-carotene and gut microflora using an in vitrofermentation model. After 24 h fermentation, the degradation rate of β-carotene was (64.28 ± 6.23)%, which was 1.46 times that of the group without gut microflora. Meanwhile, the production of VA was nearly 2 times that of the group without gut microflora, indicating that the gut microflora can metabolize β-carotene into VA. β-Carotene also influences the production of short-chain fatty acids (SCFAs), the production of total SCFAs in 0.5 mg/mL β-carotene (BCM) group was (44.00 ± 1.16) mmol/L, which was 2.26 times that of the blank control (BLK) group. Among them, the production of acetic acid in BCM group was (19.06 ± 0.82) mmol/L, which was 2.64 time that of the BLK group. Furthermore, β-carotene significantly affected the structure and composition of gut microflora, increasing the abundance of Roseburia, Parasutterellaand Lachnospiraceae, and decreasing the abundance of Dialister, Collinsellaand Enterobacter(P< 0.05). This study provides a new way to understand how β-carotene works in human body with gut microflora.