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[Display omitted] Gold nanoparticles (AuNPs) exhibit promising potential as medical materials due to their high biocompatibility, tunable size and shape, and excellent drug delivery capabilities, among other unique physicochemical properties. Previous studies have indicated the remarkable anti-inflammatory activity of ginsenoside compound K (CK). However, the relatively low bioavailability of CK restricts its effective delivery and action within the biological system. Hence, exploring novel delivery methods based on gold nanoparticles emerges as a promising strategy to overcome these challenges in application, thereby enhancing the therapeutic effectiveness of CK. Probiotic-mediated AuNPs were synthesized using gold salt and the lysates of Bifidobacterium animalis subsp. lactis. Then, CK was loaded with AuNPs to form Bifidobacterium CK AuNPs (Bifi-CKAuNPs). The anti-inflammatory activity of Bifi-CKAuNPs was evaluated in vitro using RAW 264.7 cells and in vivo using mice. The NF-κB/ mitogen-activated protein kinases (MAPK) pathway was investigated as a potential mechanism of action. In vitro experiments showed that Bifi-CKAuNPs inhibited the activation of reactive oxygen species and reduced the expression of iNOS, COX-2, and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in RAW 264.7 cells. In vivo experiments showed that Bifi-CKAuNPs significantly reduced inflammation in the lung, kidney, and liver tissues of mice without toxicity. The anti-inflammatory activity of Bifi-CKAuNPs was mediated through the inhibition of NF-κB/MAPK signal transduction, which is a well-known and critical pathway in the pathogenesis of inflammation. We have successfully synthesized and characterized Bifi-AuNPs, demonstrating its potent anti-inflammatory activity both in vitro and in vivo. Our results indicated that the NF-κB/MAPK pathway might play a key role in the mechanism of action of Bifi-CKAuNPs. These findings underscored the significant potential of Bifi-CKAuNPs as a promising platform for drug delivery and anti-inflammatory therapy. The observed efficacy in both cellular and animal models, along with insights into the underlying molecular pathways, positions Bifi-CKAuNPs as a valuable candidate for advancing therapeutic strategies in the realm of inflammation management. [ABSTRACT FROM AUTHOR]

Background: Leaky gut symptoms and inflammatory bowel disease (IBD) are associated with damaged intestinal mucosa, intestinal permeability dysfunction by epithelial cell cytoskeleton contraction, disrupted intercellular tight junction (TJ) protein expression, and abnormal immune responses and are intractable diseases.Purpose: We evaluated the effects of schisandrin C, a dibenzocyclooctadiene lignan from Schisandra chinensis, on intestinal inflammation and permeability dysfunction in gut mimetic systems: cultured intestinal cells, intestinal organoids, and a Caenorhabditis elegans model.Methods: Schisandrin C was selected from 9 lignan compounds from S. chinensis based on its anti-inflammatory effects in HT-29 human intestinal cells. IL-1β and Pseudomonas aeruginosa supernatants were used to disrupt intestinal barrier formation in vitro and in C. elegans, respectively. The effects of schisandrin C on transepithelial electrical resistance (TEER) and intestinal permeability were evaluated in intestinal cell monolayers, and its effect on intestinal permeability dysfunction was tested in mouse intestinal organoids and C. elegans by measuring fluorescein isothiocyanate (FITC)-dextran efflux. The effect of schisandrin C on TJ protein expression was investigated by western blotting and fluorescence microscopy. The signaling pathway underlying these effects was also elucidated.Results: Schisandrin C ameliorated intestinal permeability dysfunction in three IBD model systems and enhanced epithelial barrier formation via upregulation of ZO-1 and occludin in intestinal cell monolayers and intestinal organoids. In Caco-2 cells, schisandrin C restored IL-1β-mediated increases in MLCK and p-MLC expression, in turn blocking cytoskeletal contraction and subsequent intestinal permeabilization. Schisandrin C inhibited NF-ĸB and p38 MAPK signaling, which regulates MLCK expression and structural reorganization of the TJ complex in Caco-2 cells. Schisandrin C significantly improved abnormal FITC-dextran permeabilization in both intestinal organoids and C. elegans.Conclusion: Schisandrin C significantly improves abnormal intestinal permeability and regulates the expression of TJ proteins, long MLCK, p-MLC, and inflammation-related proteins, which are closely related to leaky gut symptoms and IBD development. Therefore, schisandrin C is a candidate to treat leaky gut symptoms and IBDs. [ABSTRACT FROM AUTHOR]

• Small black bean extract affects the gut microbiome in ovariectomized mice. • Small black bean extract intake decreases body weight gain in ovariectomized mice. • Small black bean extract intake ameliorates the intestinal microbial perturbation. • Small black bean extract intake also changes the intestinal metabolic status. Phytoestrogen is considered a promising natural remedy for various postmenopausal symptoms. However, most studies have focused on common soybean, Glycine max. Here, for the first time, we evaluated the in vivo effect of a distinct species, small black bean (Rhynchosia volubilis), on ovariectomized mice and investigated its impact on the intestinal microbiota and metabolic status. Ovariectomized mice exhibited significant body weight gain, a typical postmenopausal symptom, and microbial changes, such as decreased α-diversity; changes in microbial composition, especially abundances of the families Desulfovibrionaceae and Mogibacteriaceae and genus Dorea ; and decreased amino acid and short-chain fatty acid levels. Administration of small black bean extract restores body weight and gut microbial perturbation to levels similar to those observed under normal conditions. Our data suggest that small black bean extract is a potential candidate functional food for treating postmenopausal symptoms via remodeling of the intestinal microbiome. [ABSTRACT FROM AUTHOR]