ArticleMetabolites2022
Berberine Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis and Inhibits the Secretion of Gut Lysozyme via Promoting Autophagy.
Article in Metabolites, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Article
- Study on the mechanism of action of HuaZhuoKeLi in modulating LCN2-mediated cellular pyroptosis to ameliorate ulcerative colitis.Scientific reports · 2026Article
- Targeted delivery of berberineNanoscale advances · 2026Article
- Targeting mitochondrial dysfunction with traditional Chinese medicine for inflammatory bowel disease: a comprehensive review.Frontiers in pharmacology · 2026Review
- Therapeutic Agents Targeting the Nrf2 Signaling Pathway to Combat Oxidative Stress and Intestinal Inflammation in Veterinary and Translational Medicine.Veterinary sciences · 2025Review
- Camel milk and fermented camel milk prevent dextran sulfate sodium-induced ulcerative colitis via the intestinal flora-short-chain fatty acids-mucosal barrier axis in mice.Frontiers in microbiology · 2025Article
- Berberine pharmacological properties and therapeutic potential across cancer, digestive, metabolic, cardiovascular, and neurological diseases: an update review.EXCLI journal · 2025Review
- Esketamine Regulates Mitophagy through ULK1/FUNDC1 Signaling Pathway to Improve LPS-induced Acute Respiratory Distress Syndrome.Current pharmaceutical design · 2025Article
- Tocilizumab unfolds colo-protective and immunomodulatory effect in experimentally induced ulcerative colitis via mitigating autophagy and ER stress signaling.Inflammopharmacology · 2024Article
- Natural compounds target programmed cell death (PCD) signaling mechanism to treat ulcerative colitis: a review.Frontiers in pharmacology · 2024Review
- Harnessing nature's pharmacy: investigating natural compounds as novel therapeutics for ulcerative colitis.Frontiers in pharmacology · 2024Review
- Exploration of Berberine Against Ulcerative Colitis via TLR4/NF-κB/HIF-1α Pathway by Bioinformatics and Experimental Validation.Drug design, development and therapy · 2024Article
- A potential therapeutic approach for ulcerative colitis: targeted regulation of mitochondrial dynamics and mitophagy through phytochemicals.Frontiers in immunology · 2024Review
- The Role of AMPK Signaling in Ulcerative Colitis.Drug design, development and therapy · 2023Review
- Paeonol Ameliorates Ulcerative Colitis in Mice by Modulating the Gut Microbiota and Metabolites.Metabolites · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Ulcerative colitis (UC) is one of the primary types of inflammatory bowel disease, the occurrence of which has been increasing worldwide. Research in recent years has found that the level of lysozyme in the feces and blood of UC patients is abnormally elevated, and the bacterial product after the action of lysozyme can be used as an agonist to recognize different cell pattern receptors, thus regulating the process of intestinal inflammation. Berberine (BBR), as a clinical anti-diarrhea and anti-inflammatory drug, has been used in China for hundreds of years. In this study, results showed that BBR can significantly inhibit the expression and secretion of lysozyme in mice. Therefore, we try to investigate the mechanism behind it and elucidate the new anti-inflammatory mechanism of BBR. In vitro, lipopolysaccharide (LPS) was used to establish an inflammatory cell model, and transcriptomic was used to analyze the differentially expressed genes (DEGs) between the LPS group and the LPS + BBR treatment group. In vivo, dextran sulfate sodium salt (DSS) was used to establish a UC mice model, and histologic section and immunofluorescence trails were used to estimate the effect of BBR on UC mice and the expression of lysozyme in Paneth cells. Research results showed that BBR can inhibit the expression and secretion of lysozyme by promoting autophagy via the AMPK/MTOR/ULK1 pathway, and BBR promotes the maturation and expression of lysosomes. Accordingly, we conclude that inhibiting the expression and secretion of intestinal lysozyme is a new anti-inflammatory mechanism of BBR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.