scholarly journals Efficient Attenuation of Dextran Sulfate Sodium-Induced Colitis by Oral Administration of 5,6-Dihydroxy-8Z,11Z,14Z,17Z-eicosatetraenoic Acid in Mice

2021 ◽  
Vol 22 (17) ◽  
pp. 9295
Author(s):  
Shinya Takenouchi ◽  
Daiki Imai ◽  
Tatsuro Nakamura ◽  
Takahisa Murata
Keyword(s):  
Oral Administration ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Therapeutic Potential ◽  
Plasma Concentrations ◽  
Eicosatetraenoic Acid ◽  
Lipid Mediator ◽  
Granulocyte Infiltration ◽  
Mucosal Erosion ◽  
Inflammatory Bowel

5,6-dihydroxy-8Z,11Z,14Z,17Z-eicosatetraenoic acid (5,6-DiHETE) is an eicosapentaenoic acid-derived newly discovered bioactive anti-inflammatory lipid mediator having diverse functions. Here, we assessed the potential of orally administered 5,6-DiHETE in promoting healing of dextran sulfate sodium (DSS)-induced colitis in mice. We measured the plasma concentrations of 5,6-DiHETE in untreated mice before and 0.5, 1, 3, and 6 h after its oral administration (150 or 600 μg/kg) in mice. Mice developed colitis by DSS (2% in drinking water for 4 days), and 5,6-DiHETE (150 or 600 μg/kg/day) was orally administered from day 9 to 14. Next, the faecal hardness and bleeding were assessed, and the dissected colons on day 14 via H&E staining. The plasma concentration of 5,6-DiHETE reached 25.05 or 44.79 ng/mL 0.5 h after the administration of 150 or 600 μg/kg, respectively, followed by a gradual decrease. The half-life of 5,6-DiHETE was estimated to be 1.25–1.63 h. Diarrhoea deteriorated after day 3 and peaked on day 5, followed by a gradual recovery. Histological assessment on day 14 showed DSS-mediated granulocyte infiltration, mucosal erosion, submucosal edema, and cryptal abscesses in mice. Oral administration of 150 or 600 μg/kg/day of 5,6-DiHETE accelerated the recovery from the DSS-induced diarrhoea and significantly ameliorated colon inflammation. The therapeutic effect of 600 μg/kg/day 5,6-DiHETE was slightly stronger than that by 150 μg/kg/day. Our study reveals attenuation of DSS-induced colitis in mice by the oral administration of 5,6-DiHETE dose-dependently, thereby suggesting a therapeutic potential of 5,6-DiHETE for inflammatory bowel disease.

scholarly journals Prevention and Alleviation of Dextran Sulfate Sodium Salt-Induced Inflammatory Bowel Disease in Mice With Bacillus subtilis-Fermented Milk via Inhibition of the Inflammatory Responses and Regulation of the Intestinal Flora

2021 ◽  
Vol 11 ◽  
Author(s):  
Xuan Zhang ◽  
Yanjun Tong ◽  
Xiaomei Lyu ◽  
Jing Wang ◽  
Yuxue Wang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bacillus Subtilis ◽  
Inflammatory Response ◽  
Oral Administration ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Flora ◽  
Fermented Milk ◽  
Mucosal Barrier ◽  
Inflammatory Bowel

The pathogenesis of inflammatory bowel disease (IBD) might be related to the local inflammatory damage and the dysbacteriosis of intestinal flora. Probiotics can regulate the intestinal flora and ameliorate IBD. The probiotic Bacillus subtilis strain B. subtilis JNFE0126 was used as the starter of fermented milk. However, the therapeutic effects of B. subtilis-fermented milk on IBD remain to be explored. In this research, the therapeutic effect of B. subtilis-fermented milk on dextran sulfate sodium salt (DSS)-induced IBD mouse model was evaluated. Besides, the expression of pro-inflammatory/anti-inflammatory cytokines, the proliferation of the intestinal stem cells, and the reconstruction of the mucosa barrier were investigated. Finally, alteration of the gut microbiota was investigated by taxonomic analysis. As shown by the results, the disease activity index (DAI) of IBD was significantly decreased through oral administration of B. subtilis (JNFE0126)-fermented milk, and intestinal mucosa injury was attenuated. Moreover, B. subtilis could reduce the inflammatory response of the intestinal mucosa, induce proliferation of the intestinal stem cell, and promote reconstruction of the mucosal barrier. Furthermore, B. subtilis could rebalance the intestinal flora, increasing the abundance of Bacillus, Alistipes, and Lactobacillus while decreasing the abundance of Escherichia and Bacteroides. In conclusion, oral administration of the B. subtilis-fermented milk could alleviate DSS-induced IBD via inhibition of inflammatory response, promotion of the mucosal barrier reconstruction, and regulation of the intestinal flora.

scholarly journals The Noncommensal Bacterium Methylococcus capsulatus (Bath) Ameliorates Dextran Sulfate (Sodium Salt)-Induced Ulcerative Colitis by Influencing Mechanisms Essential for Maintenance of the Colonic Barrier Function

2012 ◽  
Vol 79 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Charlotte R. Kleiveland ◽  
Lene T. Olsen Hult ◽  
Signe Spetalen ◽  
Magne Kaldhusdal ◽  
Trine Eker Christofferesen ◽  
...  
Keyword(s):  
Body Weight ◽  
Barrier Function ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Therapeutic Potential ◽  
Control Diet ◽  
Plasma Concentrations ◽  
Methylococcus Capsulatus ◽  
Content Type ◽  
Ad Libitum

ABSTRACTDietary inclusion of a bacterial meal has recently been shown to efficiently abolish soybean meal-induced enteritis in Atlantic salmon. The objective of this study was to investigate whether inclusion of this bacterial meal in the diet could abrogate disease development in a murine model of epithelial injury and colitis and thus possibly have therapeutic potential in human inflammatory bowel disease. C57BL/6N mice were fedad libituma control diet or an experimental diet containing 254 g/kg of body weight BioProtein, a bacterial meal consisting ofMethylococcus capsulatus(Bath), together with the heterogenic bacteriaRalstoniasp.,Brevibacillus agri, andAneurinibacillussp. At day 8, colitis was induced by 3.5% dextran sulfate sodium (DSS)ad libitumin the drinking water for 6 days. Symptoms of DSS treatment were less profound after prophylactic treatment with the diet containing the BioProtein. Colitis-associated parameters such as reduced body weight, colon shortening, and epithelial damage also showed significant improvement. Levels of acute-phase reactants, proteins whose plasma concentrations increase in response to inflammation, and neutrophil infiltration were reduced. On the other, increased epithelial cell proliferation and enhanced mucin 2 (Muc2) transcription indicated improved integrity of the colonic epithelial layer. BioProtein mainly consists ofMethylococcus capsulatus(Bath) (88%). The results that we obtained when using a bacterial meal consisting ofM. capsulatus(Bath) were similar to those obtained when using BioProtein in the DSS model. Our results show that a bacterial meal of the noncommensal bacteriumM. capsulatus(Bath) has the potential to attenuate DSS-induced colitis in mice by enhancing colonic barrier function, as judged by increased epithelial proliferation and increased Muc2 transcription.

scholarly journals Longitudinal Microbiome Analysis in a Dextran Sulfate Sodium-Induced Colitis Mouse Model

2021 ◽  
Vol 9 (2) ◽  
pp. 370
Author(s):  
Hyunjoon Park ◽  
Soyoung Yeo ◽  
Seokwon Kang ◽  
Chul Sung Huh
Keyword(s):  
Mouse Model ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Bleeding ◽  
Cross Sectional ◽  
Microbiome Analysis ◽  
Inflammatory Bowel ◽  
Factor Design ◽  
The Individual

The role of the gut microbiota in the pathogenesis of inflammatory bowel disease (IBD) has been in focus for decades. Although metagenomic observations in patients/animal colitis models have been attempted, the microbiome results were still indefinite and broad taxonomic presumptions were made due to the cross-sectional studies. Herein, we conducted a longitudinal microbiome analysis in a dextran sulfate sodium (DSS)-induced colitis mouse model with a two-factor design based on serial DSS dose (0, 1, 2, and 3%) and duration for 12 days, and four mice from each group were sacrificed at two-day intervals. During the colitis development, a transition of the cecal microbial diversity from the normal state to dysbiosis and dynamic changes of the populations were observed. We identified genera that significantly induced or depleted depending on DSS exposure, and confirmed the correlations of the individual taxa to the colitis severity indicated by inflammatory biomarkers (intestinal bleeding and neutrophil-derived indicators). Of note, each taxonomic population showed its own susceptibility to the changing colitis status. Our findings suggest that an understanding of the individual susceptibility to colitis conditions may contribute to identifying the role of the gut microbes in the pathogenesis of IBD.

scholarly journals Rosa canina L. Can Restore Endoplasmic Reticulum Alterations, Protein Trafficking and Membrane Integrity in a Dextran Sulfate Sodium-Induced Inflammatory Bowel Disease Phenotype

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 441
Author(s):  
Dalanda Wanes ◽  
Mohamad Toutounji ◽  
Hichem Sebai ◽  
Sandra Rizk ◽  
Hassan Y. Naim
Keyword(s):  
Inflammatory Bowel Disease ◽  
Endoplasmic Reticulum ◽  
Lipid Rafts ◽  
Protein Trafficking ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Membrane Integrity ◽  
Membrane Glycoproteins ◽  
Rosa Canina ◽  
Inflammatory Bowel

Rosa canina L. is a natural polyphenol-rich medicinal plant that exhibits antioxidant and anti-inflammatory activities. Recent in vivo studies have demonstrated that a methanol extract of Rosa canina L. (RCME) has reversed an inflammatory bowel disease (IBD)-like phenotype that has been triggered by dextran sulfate sodium (DSS) in mice. In the current study, we investigated the effects of RCME on perturbations of cellular mechanisms induced by DSS-treatment of intestinal Caco-2 cells, including stress response in the endoplasmic reticulum (ER), protein trafficking and sorting as well as lipid rafts integrity and functional capacities of an intestinal enzyme. 6 days post-confluent cells were treated for 24 h with DSS (3%) or simultaneously with DSS (3%) and RCME (100 µg/mL) or exclusively with RCME (100 µg/mL) or not treated. The results obtained demonstrate the ability of RCME to counteract the substantial increase in the expression levels of several ER stress markers in DSS-treated cells. Concomitantly, the delayed trafficking of intestinal membrane glycoproteins sucrase-isomaltase (SI) and dipeptidyl peptidase 4 (DPP4) induced by DSS between the ER and the Golgi has been compromised by RCME. Furthermore, RCME restored the partially impaired polarized sorting of SI and DPP4 to the brush border membrane. An efficient sorting mechanism of SI and DPP4 is tightly associated with intact lipid rafts structures in the trans-Golgi network (TGN), which have been distorted by DSS and normalized by RCME. Finally, the enzymatic activities of SI are enhanced in the presence of RCME. Altogether, DSS treatment has triggered ER stress, impaired trafficking and function of membrane glycoproteins and distorted lipid rafts, all of which can be compromised by RCME. These findings indicate that the antioxidants in RCME act at two major sites in Caco-2 cells, the ER and the TGN and are thus capable of maintaining the membrane integrity by correcting the sorting of membrane-associated proteins.

Oat β-glucan ameliorates dextran sulfate sodium (DSS)-induced ulcerative colitis in mice

2015 ◽  
Vol 6 (11) ◽  
pp. 3454-3463 ◽  
Author(s):  
Bo Liu ◽  
Qinlu Lin ◽  
Tao Yang ◽  
Linna Zeng ◽  
Limin Shi ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Oral Administration ◽  
Inflammatory Cytokines ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Tnf Α

Oral administration of oat β-glucan ameliorates DSS induced colitis in mice by decreasing the expression of inflammatory cytokines TNF-α, IL-1β, IL-6 and iNOS.

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 Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ

PPAR Research ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Rui Kong ◽  
Hui Luo ◽  
Nan Wang ◽  
Jingjing Li ◽  
Shizan Xu ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Peroxisome Proliferator ◽  
Potential Candidate ◽  
Inflammatory Bowel ◽  
Peroxisome Proliferator Activated Receptors ◽  
Induced Apoptosis ◽  
Inflammatory Effect

Portulaca oleracea L. is a traditional Chinese medicine, which has been used as adjuvant therapy for inflammatory bowel disease (IBD). However, the mechanism of its activity in IBD still remains unclear. Since previous studies have documented the anti-inflammatory effect of peroxisome proliferator activated receptors-γ (PPAR-γ), Portulaca regulation of PPAR-γ in inflammation was examined in current study. Ulcerative colitis (UC) was generated by 5% dextran sulfate sodium (DSS) in mice and four groups were established as normal control, DSS alone, DSS plus mesalamine, and DSS plus Portulaca. Severity of UC was evaluated by body weight, stool blood form, and length of colorectum. Inflammation was examined by determination of inflammatory cytokines (TNF-a, IL-6, and IL-1a). Portulaca extract was able to attenuate development of UC in DSS model similar to the treatment of mesalazine. Moreover, Portulaca extract inhibited proinflammatory cytokines release and reduced the level of DSS-induced NF-κB phosphorylation. Furthermore, Portulaca extract restored PPAR-γ level, which was reduced by DSS. In addition, Portulaca extract protected DSS induced apoptosis in mice. In conclusion, Portulaca extract can alleviate colitis in mice through regulation of inflammatory reaction, apoptosis, and PPAR-γ level; therefore, Portulaca extract can be a potential candidate for the treatment of IBD.

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