ArticleFrontiers in nutrition2025
Aurantii Fructus extract alleviates DSS-induced colitis in mice via regulating NF-κB and Nrf2/HO-1 signaling pathways and modulating intestinal microbiota.
Article in Frontiers in nutrition, 2025. 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.
- Poricoic acid A administered during DSS exposure attenuates acute colitis in mice and is accompanied by barrier-associated changes and endpoint fecal microbiota shifts.Journal of natural medicines · 2026Article
- Activation of the Nrf2 Signaling Pathway by a Ginseng-Salvia Root-Notoginseng Composite Alleviates Ulcerative DSS-Induced Colitis via Restoring Gut Microbiota and the Intestinal Barrier.Antioxidants (Basel, Switzerland) · 2026Article
- Therapeutic Agents Targeting the Nrf2 Signaling Pathway to Combat Oxidative Stress and Intestinal Inflammation in Veterinary and Translational Medicine.Veterinary sciences · 2025Review
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7 authors.
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Abstract
Background: Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by progressive loss of intestinal function, highlighting an urgent need for effective therapeutics. This study aimed to investigate the protective effects of Aurantii Fructus extract (AFE) on dextran sulfate sodium (DSS)-induced UC in mice and its impact on the gut microbiota. Methods: The chemical components of AFE were identified using high-performance liquid chromatography (HPLC). A murine model of DSS-induced colitis was established, and the therapeutic efficacy of AFE was assessed through the disease activity index (DAI), colon length measurement, and histopathological examination. Inflammatory status and oxidative stress markers were evaluated by enzyme-linked immunosorbent assay (ELISA) and western blotting, while the expression of tight junction proteins was analyzed via immunohistochemistry. Additionally, cecal contents were subjected to 16S rRNA gene sequencing to analyze changes in the intestinal microbiota. Results: AFE treatment significantly alleviated the severity of colitis, as evidenced by reduced DAI scores, attenuated colon shortening, and improved histopathological damage. It restored the expression of the tight junction protein ZO-1 in the colon. AFE also markedly reduced the levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) and suppressed the activation of the NF-κB pathway. Concurrently, AFE enhanced antioxidant capacity by increasing glutathione (GSH) levels, decreasing malondialdehyde (MDA), and activating the Nrf2/HO-1 signaling pathway. Furthermore, AFE treatment inhibited the proliferation of pathogenic bacteria and restored the homeostasis of the gut microbiota. Conclusion: The findings demonstrate that AFE confers a protective effect against DSS-induced UC. The underlying mechanism is associated with the inhibition of the NF-κB pathway, activation of the Nrf2/HO-1 antioxidant pathway, enhancement of the intestinal barrier, and restoration of gut microbiota homeostasis.
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