ArticleFrontiers in nutrition2024
Dietary astragalin confers protection against lipopolysaccharide-induced intestinal mucosal barrier damage through mitigating inflammation and modulating intestinal microbiota.
Article in Frontiers in nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Dietary Tartary Buckwheat Flavonoids Enhance Antioxidant Capacity and Regulate Lipid Metabolism via the AMPK Pathway in Liangshan Yanying Chickens.Veterinary sciences · 2026Article
- miR-193a-5p-mediated Inhibition of the METTL1/COX-2 axis is critical for Astragalin-induced apoptosis in cervical cancer.Scientific reports · 2025Article
- Astragalin attenuates caerulein-induced acute pancreatitis by targeting the NLRP3 signaling pathway and gut microbiota.Bioresources and bioprocessing · 2025Article
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Authors and funding
8 authors.
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Abstract
Introduction: The intestinal mucosal barrier (IMB) damage is intricately linked with the onset of numerous intestinal diseases. Astragalin (AS), a flavonoid present in numerous edible plants, exhibits notable antioxidant and anti-inflammatory properties, demonstrating a promising impact on certain intestinal ailments. In this study, our objective was to investigate the protective effects of AS and elucidate the underlying mechanisms by which it mitigates lipopolysaccharide (LPS)-induced damage to the IMB in mice. Methods: During the experimental period, mice were subjected to a 7-day regimen of AS treatment, followed by LPS injection to induce IMB damage. Subsequently, a comprehensive evaluation of relevant biological indicators was conducted, including intestinal pathological analysis, serum inflammatory factors, intestinal tight junction proteins, and intestinal microbiota composition. Results: Our results suggested that AS treatment significantly bolstered IMB function. This was evidenced by the enhanced morphology of the small intestine and the elevated expression of tight junction proteins, including ZO-1 and Claudin-1, in addition to increased levels of MUC2 mucin. Moreover, the administration of AS demonstrated a mitigating effect on intestinal inflammation, as indicated by the reduced plasma concentrations of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α. Furthermore, AS treatment exerted a positive influence on the composition of the gut microbiota, primarily by augmenting the relative abundance of beneficial bacteria (including Conclusion: AS mitigates LPS-induced IMB damage via mitigating inflammation and modulating intestinal microbiota.
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