scholarly journals Tanshinone IIA ameliorates dextran sulfate sodium-induced inflammatory bowel disease via the pregnane X receptor

2015 ◽  
pp. 6343 ◽  
Author(s):  
Xianxie Zhang ◽  
yue gao ◽  
yuguang wang ◽  
Zengchun Ma ◽  
Qiande Liang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Pregnane X Receptor ◽  
Tanshinone Iia ◽  
Inflammatory Bowel

Sucralose enhances the susceptibility of dextran sulfate sodium (DSS) induced colitis in mice with changes in gut microbiota

2021 ◽  
Author(s):  
Mengru Guo ◽  
Xinran Liu ◽  
Yiwei Tan ◽  
Fangyuan Kang ◽  
Xinghua Zhu ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Artificial Sweeteners ◽  
Epidemiological Changes ◽  
Inflammatory Bowel

Sucralose is one of the most widely used artificial sweeteners, free of nutrients and calories. It’s approval and uses correlate many of the worldwide epidemiological changes of inflammatory bowel disease...

The role of the complement and contact systems in the dextran sulfate sodium-induced colitis model: the effect of C1 inhibitor in inflammatory bowel disease

2010 ◽  
Vol 298 (6) ◽  
pp. G878-G883 ◽  
Author(s):  
Fengxin Lu ◽  
Stacey M. Fernandes ◽  
Alvin E. Davis
Keyword(s):  
Inflammatory Bowel Disease ◽  
Weight Loss ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Complement C3 ◽  
C1 Inhibitor ◽  
Inflammatory Bowel

The complement and contact systems may be involved in the pathophysiological process of inflammatory bowel disease (IBD). C1 inhibitor (C1INH) is the most important inhibitor of both the complement and contact systems. We evaluated the role of these systems and the effect of both active and inactive forms of C1INH (iC1INH) in dextran sulfate sodium (DSS)-induced colitis mouse model. Three percent DSS was used in drinking water to induce colitis in complement C3-deficient (C3−/−) mice, bradykinin type 2 receptor deficient (Bk2R−/−) mice, and C57BL/6 mice. After ten days DSS exposure, C3−/− mice exhibited markedly less weight loss than wild-type (WT) mice (12 ± 3.3% vs. 30 ± 1.2%, P < 0.05) and developed a milder disease-activity index (DAI), histological score, colon shortening, and myeloperoxidase (MPO) elevation ( P < 0.05, respectively). The Bk2R−/− mice were not protected from the disease. Seven-day treatment with either native C1INH or iC1INH reduced the severity of the disease in WT mice, as indicated by decreased weight loss (15 ± 1.8%, 14 ± 2.1% vs. 30 ± 1.2%, P < 0.05, respectively), DAI, intestinal tissue damage, and MPO elevation compared with untreated WT DSS control mice ( P < 0.05, respectively). These findings suggest that complement plays a role in the development of DSS-induced colitis and that blockade of the complement system might be useful for the acute phase of IBD treatment. C1INH, however, leads to an amelioration of DSS-induced colitis via a mechanism that does not involve the inhibition of complement or contact system activation but does result in significant suppression of leukocyte infiltration.

scholarly journals Dextran sulfate sodium mouse model of inflammatory bowel disease evaluated for systemic genotoxicity via blood micronucleus and Pig-a gene mutation assays

Mutagenesis ◽  
2020 ◽  
Vol 35 (2) ◽  
pp. 161-167
Author(s):  
Christopher Kirby ◽  
Ayesha Baig ◽  
Svetlana L Avlasevich ◽  
Dorothea K Torous ◽  
Shuchang Tian ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
High Dose ◽  
Significant Treatment ◽  
Blood Samples ◽  
Inflammatory Bowel ◽  
Blood Specimens

Abstract Inflammatory bowel disease (IBD) is an important risk factor for gastrointestinal cancers. Inflammation and other carcinogenesis-related effects at distal, tissue-specific sites require further study. In order to better understand if systemic genotoxicity is associated with IBD, we exposed mice to dextran sulfate sodium salt (DSS) and measured the incidence of micronucleated cells (MN) and Pig-a mutant phenotype cells in blood erythrocyte populations. In one study, 8-week-old male CD-1 mice were exposed to 0, 1, 2, 3 or 4% w/v DSS in drinking water. The 4-week in-life period was divided into four 1-week intervals—alternately on then off DSS treatment. Low volume blood samples were collected for MN analysis at the end of each week, and cardiac blood samples were collected at the end of the 4-week period for Pig-a analyses. The two highest doses of DSS were observed to induce significant increases in reticulocyte frequencies. Even so, no statistically significant treatment-related effects on the genotoxicity biomarkers were evident. While one high-dose mouse showed modestly elevated MN frequencies during the DSS treatment cycles, it also exhibited exceptionally high reticulocyte frequencies (e.g. 18.7% at the end of the second DSS cycle). In a second study, mice were treated with 0 or 4% DSS for 9–18 consecutive days. Exposure was continued until rectal bleeding or morbidity was evident, at which point the treatment was terminated and blood was collected for MN analysis. The Pig-a assay was conducted on samples collected 29 days after the start of treatment. The initial blood specimens showed highly elevated reticulocyte frequencies in DSS-exposed mice (mean ± SEM = 1.75 ± 0.10% vs. 13.04 ± 3.66% for 0 vs. 4% mice, respectively). Statistical analyses showed no treatment-related effect on MN or Pig-a mutant frequencies. Even so, the incidence of MN versus reticulocytes in the DSS-exposed mice were positively correlated (linear fit R2 = 0.657, P = 0.0044). Collectively, these results suggest that in the case of the DSS CD-1 mouse model, systemic effects include stress erythropoiesis but not remarkable genotoxicity. To the extent MN may have been slightly elevated in a minority of individual mice, these effects appear to be secondary, likely attributable to stimulated erythropoiesis.

scholarly journals The anti-inflammatory effect and potential mechanism of cardamonin in DSS-induced colitis

2015 ◽  
Vol 309 (7) ◽  
pp. G517-G527 ◽  
Author(s):  
Gaiyan Ren ◽  
Aning Sun ◽  
Chao Deng ◽  
Jingjing Zhang ◽  
Xiaojun Wu ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Protein Kinase ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Mitogen Activated Protein Kinase ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Mitogen Activated Protein ◽  
Inflammatory Bowel

Cardamonin is a naturally occurring chalcone with strong anti-inflammatory activity. However, the direct effect of cardamonin on intestinal inflammation remains elusive. In the present study, we found that cardamonin markedly ameliorated dextran sulfate sodium-induced mouse body weight loss, diarrhea, colon shortening, spleen swelling, and histological damage, which correlated with a decline in the activity of myeloperoxidase and the production of nitric oxide, tumor necrosis factor-α and interleukin-6 in the colon. The upregulation of toll-like receptor 4 after dextran sulfate sodium treatment was associated with an increase in the activation of myeloid differentiation factor 88, interleukin-1 receptor-associated kinase-1, nuclear factor-κB (NF-κB) p65, inhibitor κBα, and inhibitor κB kinase-α/β, as well as the mitogen-activated protein kinase molecules of extracellular signal-regulated kinase and c-Jun NH2-terminal kinase, and this upregulation was reversed by cardamonin administration. Moreover, cardamonin blocked the nuclear translocation of NF-κB p65, inhibited NF-κB-luciferase activity, and downregulated NF-κB target genes expression. The present study clearly demonstrates a beneficial effect of cardamonin on experimental inflammatory bowel disease via a mechanism associated with suppression of toll-like receptor 4 expression and inactivation of NF-κB and mitogen-activated protein kinase pathways. This study may give insight into the further evaluation of the therapeutic potential of cardamonin or its derivatives for human inflammatory bowel disease.

scholarly journals Metabolic profiling of liver in C57BL/6 mice with DSS-induced inflammatory bowel disease by untargeted metabolomics analysis

2019 ◽  
Author(s):  
Zhongquan Xin ◽  
Zhenya Zhai ◽  
Hongrong Long ◽  
Fan Zhang ◽  
Xiaojun Ni ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Metabolic Pathways ◽  
Dextran Sulfate ◽  
Acid Metabolism ◽  
Dextran Sulfate Sodium ◽  
Liver Disorder ◽  
Cecropin A ◽  
Inflammatory Bowel ◽  
Metabolomics Analysis

Abstract Background: Inflammatory bowel disease (IBD) is a systemic disease that frequently causes liver damage. However, the metabolic mechanism of liver disorder induced by IBD is still unclear. This study aimed to revile metabolic profiles of liver in mice which induced inflammatory bowel disease by dextran sulfate sodium (DSS) and treated by cecropin A and gentamicin . Methods: In this study, IBD mold mice were established, C57BL/6 mice were given water containing 2.5% dextran sulfate sodium (DSS) for 5 days. Subsequently, the mice were treated via intraperitoneally injected with saline, 15 mg/kg cecropin A, 5 mg/kg gentamicin for 3 days, respectively. The liver in IBD mold mice or treated by cecropin A and gentamicin, were performed metabolomics analysis through UPLC–Orbitrap–MS/MS. Database integration analysis software was used to identify metabolites of liver. Multivariate analysis, including principal component analysis (PCA), hierarchical cluster analysis (HCA) and orthogonal partial least-squares discriminant analysis (OPLS-DA). Furthermore, metabolic pathway analysis was performed using MetaboAnalyst 4.0. Results: A total of 133 metabolites were identified in liver of mice and 20 key metabolites were considered as potential biomarkers were identified between the control and IBD group. There are 4 key metabolic pathways include bile acid metabolism, arachidonic acid metabolism, amino acid and protein metabolism, and steroid hormone biosynthesis in liver was disturbed by IBD, and we also found that those pathways were reversed when mice were treated by cecropin A and gentamicin. Conclusion: The results indicated that those differential metabolites and metabolic pathways changed in liver were likely to be caused by IBD. The further study shall be carried out to explore the mechanism of liver disorder induced by IBD.

scholarly journals Upregulation of P-glycoprotein by probiotics in intestinal epithelial cells and in the dextran sulfate sodium model of colitis in mice

2011 ◽  
Vol 300 (6) ◽  
pp. G1115-G1123 ◽  
Author(s):  
Seema Saksena ◽  
Sonia Goyal ◽  
Geetu Raheja ◽  
Varsha Singh ◽  
Maria Akhtar ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Epithelial Cells ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Epithelial Cells ◽  
Myeloperoxidase Activity ◽  
Intestinal Epithelial ◽  
P Glycoprotein ◽  
Inflammatory Bowel

P-glycoprotein (P-gp) mediates efflux of xenobiotics and bacterial toxins from the intestinal mucosa into the lumen. Dysregulation of P-gp has been implicated in inflammatory bowel disease. Certain probiotics have been shown to be effective in treating inflammatory bowel disease. However, direct effects of probiotics on P-gp are not known. Current studies examined the effects of Lactobacilli on P-gp function and expression in intestinal epithelial cells. Caco-2 monolayers and a mouse model of dextran sulfate sodium-induced colitis were utilized. P-gp activity was measured as verapamil-sensitive [3H]digoxin transepithelial flux. Multidrug resistant 1 (MDR1)/P-gp expression was measured by real-time quantitative PCR and immunoblotting. Culture supernatant (CS; 1:10 or 1:50, 24 h) of Lactobacillus acidophilus or Lactobacillus rhamnosus treatment of differentiated Caco-2 monolayers (21 days postplating) increased (∼3-fold) MDR1/P-gp mRNA and protein levels. L. acidophilus or L. rhamnosus CS stimulated P-gp activity (∼2-fold, P < 0.05) via phosphoinositide 3-kinase and ERK1/2 MAPK pathways. In mice, L. acidophilus or L. rhamnosus treatment (3 × 109 colony-forming units) increased mdr1a/P-gp mRNA and protein expression in the ileum and colon (2- to 3-fold). In the dextran sulfate sodium (DSS)-induced colitis model (3% DSS in drinking water for 7 days), the degree of colitis as judged by histological damage and myeloperoxidase activity was reduced by L. acidophilus. L. acidophilus treatment to DSS-treated mice blocked the reduced expression of mdr1a/P-gp mRNA and protein in the distal colon. These findings suggest that Lactobacilli or their soluble factors stimulate P-gp expression and function under normal and inflammatory conditions. These data provide insights into a novel mechanism involving P-gp upregulation in beneficial effects of probiotics in intestinal inflammatory disorders.

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