In this study, the changes in total polyphenols, total flavonoids and chlorogenic acid contents during the processing of Lycium barbarum bud tea were compared and analyzed, and the metabolite composition of the tea at different processing stages was systematically analyzed by widely targeted metabolomics to clarify their effects on the chemical composition of L. barbarum bud tea. The results showed that L. barbarum buds had the highest contents of total polyphenols, (43.65 ± 3.15) mg/g, total flavonoids, (10.68 ± 0.25) mg/g, and chlorogenic acid (5.24 ± 0.52) mg/g. The contents of these phenolic substances decreased significantly (P < 0.05) as bleaching, primary fixation, secondary fixation, frying and flavoring progressed. Notably, after the secondary fixation, the contents of total polyphenols, total flavonoids and chlorogenic acid decreased by 19%, 29% and 27%, respectively. Widely targeted metabolomics identified 594 metabolites belonging to 11 categories, including flavonoids, phenolic acids, alkaloids, amino acids and their derivatives, and lipids. In total, 270, 287, 298, 295, and 298 significantly differential metabolites were identified in L. barbarum buds versus bleaching, primary fixation, secondary fixation, frying and flavoring, respectively, with the major ones being flavonoids, nucleotides and their derivatives, phenolic acid, amino acids and their derivatives. These differential metabolites were predominantly enriched in metabolic pathways such as purine metabolism, niacin and nicotinamide metabolism, cysteine and methionine metabolism, and a small proportion of them was enriched in pathways like zeeatin biosynthesis, and ABC transporter. Significant differences were observed in inosine, homocysteine, cinnamic acid, 4-hydroxy-3-methoxycinnamic acid, and isoferulic acid among processing stages, indicating their involvement in the quality formation of L. barbarum bud tea during processing. The findings of this study provide a theoretical basis for understanding the changes in nutritional and functional components and for the quality control of L. barbarum bud tea during processing.

Selenium is a crucial trace element that contributes to physiological processes in the body as selenoproteins. Selenoproteins serve as an integral role in the body in controlling the redox state of cells and protecting against damage induced by oxidative stress. This study aimed to investigate the effects and possible mechanism of selenium on selenoproteins expression in EA.hy926 cells induced by oxidized low density lipoprotein (oxLDL). The impact of selenium on the viability of EA.hy926 cells was detected by the methylthiazolyldiphenyl-tetrazolium bromide (MTT) method, and intracellular reactive oxygen species (ROS) level and mitochondrial membrane potential were assessed by fluorescent probe DCFH-DA and JC-1, respectively. RNA-seq, quantitative real-time polymerase chain reaction (qPCR), and Western blot were used to investigate the selenoprotein expression. Selenoprotein mRNA translation efficiency was analyzed by ribosome profiling (Ribo-Seq) coupled with transcriptomics. Our data showed that selenium supplementation (0.5 μmol/L) significantly decreased ROS production, increased mitochondrial inner membrane potential and increased the proliferative activity of EA.hy926 cells induced by oxLDL. Moreover, The protective effects of selenium against oxLDL-induced EA.hy926 cell injury were associated with the upregulation of the expressions of selenoproteins glutathione peroxidase 1 (GPX1), glutathione peroxidase 4 (GPX4), and thioredoxin reductase 1 (TXNRD1). Furthermore, the expressions of selenoproteins GPX1 and GPX4 were hierarchically controlled, but the expressions of selenoproteins TXNRD1 were mainly regulated by oxLDL. Finally, Ribo-Seq coupled with transcriptomics results demonstrated that the expressions of selenoproteins GPX1, GPX4, and TXNRD1 were regulated at the translation process level. These findings suggested that selenium could have preventive effects in oxLDL induced EA.hy926 cell injury by regulating the selenoprotein expression, and the selenoproteins expressions at the translation level in vascular endothelial cells need further study.

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 barbarum on 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 Lactobacillus and 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.