ArticleThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology2022
Butyrate Ameliorates Intestinal Epithelial Barrier Injury Via Enhancing Foxp3+ Regulatory T-Cell Function in Severe Acute Pancreatitis Model.
Article in The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 14 citations in OpenAlex.
- Epithelial-immune interface in asthma: Mechanistic insights driving novel therapeutic strategies.Seminars in immunopathology · 2026Review
- The Roles of Gut Microbiota in the Pathogenesis of Acute Pancreatitis.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- The role of the gut-lung axis in persistent inflammation and disease progression in chronic obstructive pulmonary disease: mechanistic evidence and therapeutic implications.Frontiers in immunology · 2026Review
- 3D vascular mapping reveals multi-organ injury following severe acute pancreatitis.Theranostics · 2026Article
- Beyond the Pancreas: The Gut Microbiota in Acute Pancreatitis - From Mechanisms to Therapeutic Perspectives.Clinical and experimental gastroenterology · 2026Review
- The role of gut microbiota in osteoporosis: underlying mechanisms, clinical associations, and emerging biomaterials.Frontiers in immunology · 2026Review
- The Microecological-Immune Axis in Pediatric Allergic Diseases: Imbalance Mechanisms and Regulatory Interventions.Nutrients · 2025Review
- Sodium Butyrate Inhibits Necroptosis by Regulating MLKL via E2F1 in Intestinal Epithelial Cells of Liver Cirrhosis.Journal of clinical and translational hepatology · 2025Article
- The role of intestinal microbiota and its metabolite short-chain fatty acids in hypertriglyceridemia-associated acute pancreatitis.Frontiers in microbiology · 2025Review
- Immune dysregulation in ulcerative colitis: pathogenic mechanisms and therapeutic strategies of traditional Chinese medicine.Frontiers in cell and developmental biology · 2025Review
- Review
- The Interaction of Microbiome and Pancreas in Acute Pancreatitis.Biomolecules · 2023Review
- The Role of Short-Chain Fatty Acids in Acute Pancreatitis.Molecules (Basel, Switzerland) · 2023Review
- Identification of Key Biomarkers Associated with Immunogenic Cell Death and Their Regulatory Mechanisms in Severe Acute Pancreatitis Based on WGCNA and Machine Learning.International journal of molecular sciences · 2023Article
- Article
- Admissions for acute biliary pancreatitis without necrosis and infection complicated by severe sepsis and septic shock: a national study.Annals of gastroenterologyArticle
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8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aimed to examine the effect of sodium butyrate on severe acute pancreatitis-related gut barrier injury in a rat model and explore its mechanism.
methodsMale rats randomly fell into 3 groups, that is, the control, the severe acute pancreatitis group, and the severe acute pancreatitis+butyrate group. Rats in the control group received sham operation, while rats in the severe acute pancreatitis group and severe acute pancreatitis+butyrate group received severe acute pancreatitis induction by intraductal infusion of 4% sodium taurocholate. After that, rats in the severe acute pancreatitis+butyrate group were fed with sodium butyrate solution with free access. Intestinal barrier injury was measured based on the expression of tight junction proteins by reverse transcription polymerase chain reaction, Western blotting assay as well as immunohistochemical staining. The variation of Treg cells was measured by reverse transcription polymerase chain reaction, Western blotting assay, immunohistochemical staining, and flow cytometry analysis.
resultsCompared to rats in the control, rats in the severe acute pancreatitis group showed significantly higher pathohistological scores (P < .001) in the intestine, as well as decreased expression of occludin and ZO-1. While, rats in the severe acute pancreatitis+butyrate group showed mitigated histologic lesions (P < .05) and increased expressions of occludin and ZO-1. In addition, rats in the severe acute pancreatitis group showed the obvious reduction in the expressions of Foxp3 and GPR109a and the decreased percentage of Treg cells in the intestine (P < .001) compared to rats in the control. However, rats in the severe acute pancreatitis+butyrate group showed markedly increased expressions of Foxp3 and GPR109a and the upregulated percentage of Treg cells (P < .01).
conclusionButyrate could significantly mitigate the intestinal injury induced by severe acute pancreatitis, probably by inducing the differentiation of Treg cells.
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