ArticleInternational journal of molecular sciences2026
Bovine Milk-Derived Extracellular Vesicles Ameliorate Steatohepatitis by Restoring Gut Barrier in CDA-HFD-Fed Mice.
Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gut barrier dysfunction and portal endotoxemia contribute to metabolic dysfunction-associated steatohepatitis (MASH) progression through activation of hepatic inflammatory signaling. Milk-derived extracellular vesicles (EVs) contain bioactive microRNAs and have recently attracted attention as modulators of intestinal homeostasis. This study investigated the effect of bovine milk-derived extracellular vesicles (B-mEVs) in ameliorating MASH by improving intestinal barrier function. C57BL/6J mice fed a choline-deficient amino acid-defined high-fat diet (CDA-HFD) were orally treated with B-mEVs, and therapeutic effects were evaluated. Liver histology, fibrosis, portal lipopolysaccharide (LPS) levels, intestinal permeability, and gut microbiota composition were evaluated. The direct effects of B-mEVs on intestinal barrier function were assessed using palmitic acid-stimulated Caco-2 cells. Small RNA sequencing and microRNA enrichment analyses were performed to characterize B-mEV cargo. B-mEV treatment attenuated hepatic steatosis, inflammation, and fibrosis in CDA-HFD-fed mice and reduced serum aminotransferase levels, portal LPS concentrations, hepatic macrophage accumulation, and hepatic TLR4/NF-κB signaling activation. Meanwhile, B-mEVs restored intestinal tight junction proteins, including ZO-1, occludin, and claudin-1, and improved intestinal permeability in vivo. In Caco-2 cells, B-mEVs attenuated palmitic acid-induced barrier dysfunction and suppressed myosin light chain kinase expression. Gut microbiota analysis revealed partial restoration of
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