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Dextran sodium sulfate colitis murine model: An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis

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World Journal of Gastroenterology 2017年第33期23卷 6016-6029页

作者： Derrick D Eichele Kusum K Kharbanda Department of Internal Medicine Nebraska Medical Center Research Service Veterans Affairs Nebraska-Western Iowa Health Care System Department of Biochemistry and Molecular Biology Nebraska Medical Center

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 respon-se in a genetically susceptible host due to inciting environmental factors occurs. To investigate the path-ogenesis 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.

关键词： Dextran sodium sulfate Experimental colitis Inflammatory bowel disease Pathogenesis Intestinal barrier

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Lysophosphatidic acid increases SLC26A3 expression in inflamed intestine and reduces diarrheal severity in C57BL/6 mice with dextran-sodium-sulfate-induced colitis

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Chinese Medical Journal 2014年第9期127卷 1737-1743页

作者： Xu Lihong Xiao Fang He Jiayi Lan Xiaoqin Ding Qiang Li Junhua Ursula Seidler Zheng Yong Tian Dean Department of Gastroenterology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China Department of Gastroenterology Hannover Medical School 30625Hannover Germany Department of Nephrology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China Department of Gastroenterology First Affiliated Hospital ShiheziSchool of Medicine Shihezi University Shihezi Xinjiang Uygur Autonomous Region 832008 China

Background Diarrhea is a common clinical feature of ulcerative colitis resulting from unbalanced intestinal fluid and salt absorption and secretion.The Cl-/HCO3-exchanger SLC26A3 is strongly expressed in the mid-distal colon and plays an essential role in colonic Cl-absorption and HCO3-secretion.Sic26a3 expression is up-regulated by lysophosphatidic acid （LPA） in vitro.Our study was designed to investigate the effects of LPA on SLC26A3 expression and the diarrheal phenotype in a mouse colitis model.Methods Colitis was induced in C57BL/6 mice by adding 4％ of Dextran sodium sulfate （DSS） to the drinking water.The mice were assigned to LPA treatment DSS group,phosphate-buffered saline （PBS） treatment DSS group,DSS only group and untreated mice with a completely randomized design.Diarrhea severity was evaluated by measuring mice weight,disease activity index （DAI）,stool water content and macroscopic evaluation of colonic damage.The effect of LPA treatment on Sic26a3 mRNA level and protein expression in the different groups of mice was investigated by quantitative PCR and Western blotting.Results All mice treated with DSS lost weight,but the onset and severity of weight loss was attenuated in the LPA treatment DSS group.The increases in stool water content and the macroscopic inflammation score in LPA treatment DSS group were significantly lower compared to DSS control group or PBS treatment DSS group （（18.89±8.67）％ vs.（28.97±6.95）％ or （29.48±6.71）％,P=0.049,P=0.041,respectively and 2.67±0.81 vs.4.5±0.83 or 4.5±0.54,P=0.020,P=0.006,respectively）,as well as the increase in DAI （P=0.004,P=0.008,respectively）.LPA enema resulted in higher Slc26a3 mRNA and protein expression levels compared to PBS-treated and untreated DSS colitis mice.Conclusion LPA increases Slc26a3 expression in the inflamed intestine and reduces diarrhea severity in DSS-induced colitis,suggesting LPA might be a therapeutic strategy in the treatment of colitis associated diarrhea.

关键词： lysophosphatidic acid SLC26A3 antidiarrheals Dextran sodium sulfate colitis

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3,6-dichlorobenzo[b]thiophene-2-carboxylic acid alleviates ulcerative colitis by suppressing mammalian target of rapamycin complex 1 activation and regulating intestinal microbiota

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World Journal of Gastroenterology 2022年第46期28卷 6522-6536页

作者： Qiong-Zi He Peng Wei Jun-Zhi Zhang Tong-Tong Liu Kun-Qun Shi Huan-Huan Liu Jing-Wei Zhang Shi-Jia Liu Affiliated Hospital of Nanjing University of Chinese Medicine Jiangsu Province Hospital of Chinese MedicineNanjing 210029Jiangsu ProvinceChina College of The First Clinical Medicine Nanjing University of Chinese MedicineNanjing 210023Jiangsu ProvinceChina School of Life Science and Technology China Pharmaceutical UniversityNanjing 211198Jiangsu ProvinceChina

BACKGROUND 3,6-dichlorobenzo[b]thiophene-2-carboxylic acid(BT2)is a benzothiophene carboxylate derivative that can suppress the catabolism of branched-chain amino acid(BCAA)-associated mammalian target of rapamycin complex 1(mTORC1)activation.Previous studies have demonstrated the therapeutic effects of BT2 on arthritis,liver cancer,and kidney injury.However,the effects of BT2 on ulcerative colitis(UC)are unknown.AIM To investigate the anti-UC effects of BT2 and the underlying mechanism.METHODS Mouse UC models were created through the administration of 3.5%Dextran sodium sulfate(DSS)for 7 d.The mice in the treated groups were administered salazosulfapyridine(300 mg/kg)or BT2(20 mg/kg)orally from day 1 to day 7.At the end of the study,all of the mice were sacrificed,and colon tissues were removed for hematoxylin and eosin staining,immunoblot analyses,and immunohistochemical assays.Cytokine levels were measured by flow cytometry.The contents of BCAAs including valine,leucine,and isoleucine,in mouse serum were detected by liquid chromatography-tandem mass spectrometry,and the abundance of intestinal flora was analyzed by 16S ribosomal DNA sequencing.RESULTS Our results revealed that BT2 significantly ameliorated the inflammatory symptoms and pathological damage induced by DSS in mice.BT2 also reduced the production of the proinflammatory cytokines interleukin 6(IL-6),IL-9,and IL-2 and increased the anti-inflammatory cytokine IL-10 level.In addition,BT2 notably improved BCAA catabolism and suppressed mTORC1 activation and cyclooxygenase-2 expression in the colon tissues of UC mice.Furthermore,highthroughput sequencing revealed that BT2 restored the gut microbial abundance and diversity in mice with colitis.Compared with the DSS group,BT2 treatment increased the ratio of Firmicutes to Bacteroidetes and decreased the abundance of Enterobacteriaceae and Escherichia-Shigella.CONCLUSION Our results indicated that BT2 significantly ameliorated DSS-induced UC and that the latent mechanism involved the suppression of BCAA-as

关键词： 3,6-dichlorobenzo[b]thiophene-2-carboxylic acid Ulcerative colitis Mechanistic target of rapamycin complex 1 Intestinal flora Dextran sodium sulfate Cyclooxygenase-2

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Cortical Inflammation is Increased in a DSS-Induced Colitis Mouse Model

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Neuroscience Bulletin 2018年第6期34卷 1058-1066页

作者： Ying Han Tong Zhao Xiang Cheng Ming Zhao Sheng-Hui Gong Yong-Qi Zhao Hai-Tao Wu Ming Fan Ling-Ling Zhu Center for Brain Disorders Research Capital Medical University Beijing Institute of Brain Disorders Institute of Military Cognition and Brain Sciences Academy of Military Medical Sciences Co-innovation Center of Neuroregeneration Nantong University

While inflammatory bowel disease(IBD) might be a risk factor in the development of brain dysfunctions,the underlying mechanisms are largely unknown. Here,mice were treated with 5% Dextran sodium sulfate(DSS) in drinking water and sacrificed on day 7. The serum level of IL-6 increased, accompanied by elevation of the IL-6 and TNF-a levels in cortical tissue. However, the endotoxin concentration in plasma and brain of mice with DSSinduced colitis showed a rising trend, but with no significant difference. We also found significant activation of microglial cells and reduction in occludin and claudin-5 expression in the brain tissue after DSS-induced colitis.These results suggested that DSS-induced colitis increases systemic inflammation which then results in cortical inflammation via up-regulation of serum cytokines. Here,we provide new information on the impact of colitis on the outcomes of cortical inflammation.

关键词： Cortical inflammation Dextran sodium sulfate Colitis Endotoxin Blood-brain barrier

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