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Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are complex diseases that result from the chronic dysregulated immune response in the gastrointestinal tract. The exact etiology is not fully understood, but it is accepted that it occurs when an inappropriate aggressive inflammatory response in a genetically susceptible host due to inciting environmental factors occurs. To investigate the pathogenesis and etiology of human IBD, various animal models of IBD have been developed that provided indispensable insights into the histopathological and morphological changes as well as factors associated with the pathogenesis of IBD and evaluation of therapeutic options in the last few decades. The most widely used experimental model employs dextran sodium sulfate (DSS) to induce epithelial damage. The DSS colitis model in IBD research has advantages over other various chemically induced experimental models due to its rapidity, simplicity, reproducibility and controllability. In this manuscript, we review the newer publicized advances of research in murine colitis models that focus upon the disruption of the barrier function of the intestine, effects of mucin on the development of colitis, alterations found in microbial balance and resultant changes in the metabolome specifically in the DSS colitis murine model and its relation to the pathogenesis of IBD.
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http://dx.doi.org/10.3748/wjg.v23.i33.6016 | DOI Listing |
J Agric Food Chem
September 2025
College of Food Science and Engineering, Northwest A&F University, Yangling 712100, China.
Dietary proteins have been demonstrated to alleviate ulcerative colitis. Phosvitin (PSV), a highly phosphorylated protein, possesses biological functions such as anti-inflammatory and antioxidant activities. This study aimed to investigate the preventive effects of PSV on dextran sulfate sodium (DSS)-induced colitis in mice and its underlying mechanisms.
View Article and Find Full Text PDFInflamm Bowel Dis
September 2025
Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.
Background: Ulcerative colitis (UC) is a gastrointestinal inflammatory condition with an unclear etiology. Recent findings suggest that metabolites play a pivotal role in promoting intestinal health. We have previously observed a significant enrichment in colonic branched-chain amino acids (BCAAs) in resistant mice to colitis suggesting the potential role of these metabolites in UC development.
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
The Second Department of Gastroenterology, Shengjing Hospital of China Medical University, No. 36, Sanhao Road, Heping District, Shenyang 110000, Liaoning, China. Electronic address:
Purpose: This study aimed to elaborate the mechanism of cuproptosis induced by HO in ulcerative colitis (UC).
Methods: Bioinformatics based on GSE107499, GSE87466, and GSE92415 datasets was performed to screen hub genes related to cuproptosis. In vitro, cell counting kit 8 (CCK8), flow cytometry were applied for detecting cell proliferation and apoptosis.
Am J Physiol Regul Integr Comp Physiol
September 2025
Laboratory of Anesthesia and Critical Care Medicine, National-Local Joint Engineering Research Centre of Translational Medicine of Anesthesiology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Ulcerative colitis (UC) is a serious inflammatory bowel disease with a significantly increasing incidence globally. Current treatment options often exhibit unstable efficacy and notable side effects, making the exploration of alternative therapies particularly important. Peucedanum praeruptorum Dunn, a traditional Chinese medicine, contains various bioactive compounds, among which praeruptorin A (PA) has garnered attention for its anti-inflammatory potential.
View Article and Find Full Text PDFActa Biochim Biophys Sin (Shanghai)
September 2025
State Key Laboratory of Analytical Chemistry for Life Sciences, School of Life Sciences, Nanjing University, Nanjing 210023, China.
Dysregulated transcription factors critically link chronic inflammation to oncogenesis in colitis-associated colorectal cancer (CAC), but their mechanistic roles remain incompletely understood. By integrating microarray and transcriptome sequencing data from ulcerative colitis (UC), colitis-associated cancer (CAC), and colorectal cancer (CRC) patients, we identify C/EBPβ as a key transcriptional regulator whose elevated expression inversely correlates with survival. In azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced CAC models, intestinal epithelial C/EBPβ is upregulated during tumor progression, which is correlated with exacerbated tumor burden and neutrophil infiltration.
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