ArticleFrontiers in microbiology2024
Intestinal and hepatic benefits of BBR-EVO on DSS-induced experimental colitis in mice.
Article in Frontiers in microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Use of Antihistamine Drugs in Colitis: A Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Berberine in Inflammatory Bowel Disease: Integrative Regulation of the Microbiota-Immune-Barrier Axis.International journal of molecular sciences · 2026Review
- Mechanisms and therapeutic potential of traditional Chinese medicine for inflammatory bowel disease.World journal of gastroenterology · 2026Review
- The Impact of H1-H4 Receptor Antagonists on the Levels of Selected Oxidative Stress Markers in Liver and Muscle Tissue in an Animal Model of Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- MODULATING OXIDATIVE STRESS AND INFLAMMATION: SODIUM BUTYRATE'S THERAPEUTIC PROMISE IN EXPERIMENTAL COLITIS.Arquivos de gastroenterologia · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Ulcerative colitis (UC), characterized by disrupted intestinal barrier integrity and chronic inflammation, was modeled in mice via dextran sulfate sodium (DSS) induction. This study explored the therapeutic potential of berberine-evodiamine (BBR-EVO), bioactive components of the traditional Chinese medicine Yulian decoction, in DSS colitis. BBR-EVO intervention ameliorated weight loss, diarrhea, colonic shortening, and histopathological damage in colitic mice. The substance increased antioxidant activity while reducing high levels of pro-inflammatory cytokines in the colon, including as TNF-α, IL-1β, and IL-6. BBR-EVO inhibited the DSS-induced decrease in the tight junction proteins ZO-1 and occludin, according to immunohistochemistry. 16S rRNA sequencing demonstrated BBR-EVO partially attenuated DSS-elicited intestinal dysbiosis, reducing opportunistic pathogens and restoring diminished beneficial taxa. Critically, BBR-EVO alleviated secondary hepatic injury in colitic mice, mitigating immune cell infiltration, oxidative stress, cytokine production, and ultrastructural damage, likely by beneficially modulating gut-liver crosstalk. This study reveals BBR-EVO, derived from a traditional Chinese medicine, confers multi-target protective effects in experimental colitis and associated hepatic pathology, warranting further evaluation as a potential therapy for inflammatory bowel diseases like UC. The mechanisms may involve simultaneous augmentation of intestinal barrier integrity, inhibition of inflammation, microbiota regulation, and gut-liver axis optimization.
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