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A functional food formula named SVS consists of serum-derived bovine immunoglobulin protein isolate, vitamin C, and selenium-enriched yeast. Here, we aimed to investigate the immunoregulatory effects of SVS in vivo and to elucidate its underlying mechanism. In normal mice, administration of SVS significantly enhanced delayed-type hypersensitivity responses, increased hemolysis plaque counts, and elevated serum hemolysin levels, indicating boosted cellular and humoral immunity. Furthermore, in a murine model of exercise-induced immunosuppression, SVS administration resulted in reduced serum BUN levels and increased IgG concentrations, suggesting a dual role in alleviating fatigue and enhancing immune function. Additionally, SVS balanced T cell differentiation by increasing IFN-γ levels while decreasing IL-4 levels. Gut microbiota analysis showed that SVS increased species diversity in immunosuppressed mice. Notably, an increase in the abundance of beneficial bacterial taxa was observed, specifically including Bacteroides, Akkermansia, and Lachnospiraceae_NK4A136_group. Metabolomic analysis revealed that SVS reversed immunosuppression-induced disturbances in metabolites, particularly in sphingolipid and glycerophospholipid pathways. Correlation analysis suggested that the immune-enhancing effects of SVS are linked to its regulatory impact on gut microbiota and metabolism. These findings support the potential of SVS as a therapeutic immune-enhancing health food.

Alzheimer’s disease (AD) is a neurodegenerative disorder associated with age. A wealth of evidence indicates that the amyloid β (Aβ) aggregates result from dyshomeostasis between Aβ production and clearance, which plays a pivotal role in the pathogenesis of AD. Consequently, therapies targeting Aβ reduction represent a promising strategy for AD intervention. Tetramethylpyrazine nitrone (TBN) is a novel tetramethylpyrazine derivative with potential for the treatment of AD. Previously, we demonstrated that TBN markedly enhanced cognitive functions and decreased the levels of Aβ, APP, BACE 1, and hyperphosphorylated tau in 3×Tg-AD mice. However, the mechanism by which TBN inhibits Aβ deposition is still unclear. In this study, we employed APP/PS1 mice treated with TBN (60 mg/kg, ig, bid) for six months, and N2a/APP695swe cells treated with TBN (300 μM) to explore the mechanism of TBN in Aβ reduction. Our results indicate that TBN significantly alleviated cognitive impairment and reduced Aβ deposition in APP/PS1 mice. Further investigation of the underlying mechanisms revealed that TBN decreased the expression of APP and BACE1, activated the AMPK/mTOR/ULK1 autophagy pathway, inhibited the PI3K/AKT/mTOR/ULK1 autophagy pathway, and decreased the phosphorylation levels of JNK and ERK in APP/PS1 mice. Moreover, TBN was found to significantly reduce the mRNA levels of APP and BACE1, as well as those of SP1, CTCF, TGF-β, and NF-κB, transcription factors involved in regulating gene expression. Additionally, TBN was observed to decrease the level of miR-346 and increase the levels of miR-147 and miR-106a in the N2a/APP695swe cells. These findings indicate that TBN may reduce Aβ levels likely by reducing APP expression by regulating APP gene transcriptional factors and miRNAs, reducing BACE1 expression, and promoting autophagy activities.