Effects of dextran sodium sulfate on normal colonic tissue and tumors in wild type and Apc-Pirc/+ rats.
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE54036 | GEO | 2014/01/14
SECONDARY ACCESSION(S): PRJNA234470
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-01-14 | E-GEOD-54036 | biostudies-arrayexpress
Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine which genes are altered in the normal colonic epithelium, and which changes depend on the Pirc mutation.
2014-01-14 | GSE54005 | GEO
Project description:Effects of dextran sodium sulfate on normal colonic tissue and tumors in wild type and Apc-Pirc/+ rats.
| PRJNA234470 | ENA
Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine which genes are altered in the normal colonic epithelium, and which changes depend on the Pirc mutation. 97 day old (ACIxF344)F1 wild type and Pirc male rats either untreated or given 4% DSS in the drinking water from 40-47 and 54-61 days of age, housed in 12 hour light:12 dark, ad lib feeding. Normal colonic tissue was collected from the distal colon at 97 days of age.
2014-01-14 | E-GEOD-54005 | biostudies-arrayexpress
Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine whether genes altered in the normal colonic epithelium or tumor differed between sporadic and inflammation-associated tumor development.
2014-01-14 | GSE54035 | GEO
Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine whether genes altered in the normal colonic epithelium or tumor differed between sporadic and inflammation-associated tumor development. 97 day old (ACIxF344)F1-Pirc male rats either untreated or given 4% DSS in the drinking water from 40-47 and 54-61 days of age, housed in 12 hour light:12 dark, ad lib feeding and drinking conditions. Normal colonic tissue and tumors were harvested from the distal colon at 97 days of age. A two color, reference design experiment hybridized according to Agilent protocols against a reference pool of RNA made up from colon tissue taken from pooled wild type rats which was labeled with Cy5.
2014-01-14 | E-GEOD-54035 | biostudies-arrayexpress
Project description:BackgroundDisruption of central circadian rhythms likely mediated by changes in microbiota and a decrease in gut-derived metabolites like short chain fatty acids (SCFAs) negatively impacts colonic barrier homeostasis. We aimed to explore the effects of isolated peripheral colonic circadian disruption on the colonic barrier in a mouse model of colitis and explore the mechanisms, including intestinal microbiota community structure and function.MethodsColon epithelial cell circadian rhythms were conditionally genetically disrupted in mice: TS4Cre-BMAL1lox (cBMAL1KO) with TS4Cre as control animals. Colitis was induced through 5 days of 2% dextran sulfate sodium (DSS). Disease activity index and intestinal barrier were assessed, as were fecal microbiota and metabolites.ResultsColitis symptoms were worse in mice with peripheral circadian disruption (cBMAL1KO). Specifically, the disease activity index and intestinal permeability were significantly higher in circadian-disrupted mice compared with control animals (TS4Cre) (P < .05). The worsening of colitis appears to be mediated, in part, through JAK (Janus kinase)-mediated STAT3 (signal transducer and activator of transcription 3), which was significantly elevated in circadian-disrupted (cBMAL1KO) mice treated with DSS (P < .05). Circadian-disrupted (cBMAL1KO) mice also had decreased SCFA metabolite concentrations and decreased relative abundances of SCFA-producing bacteria in their stool when compared with control animals (TS4Cre).ConclusionsDisruption of intestinal circadian rhythms in colonic epithelial cells promoted more severe colitis, increased inflammatory mediators (STAT3 [signal transducer and activator of transcription 3]), and decreased gut microbiota-derived SCFAs compared with DSS alone. Further investigation elucidating the molecular mechanisms behind these findings could provide novel circadian directed targets and strategies in the treatment of inflammatory bowel disease.
| S-EPMC9977234 | biostudies-literature
Project description:Oleoylethanolamide (OEA) is an endogenous fatty acid ethanolamide known for its anti-inflammatory effects and its influence on gut microbiota composition; however, the effects of OEA in inflammatory bowel disease (IBD) remain unknown. During in vitro experiments, OEA downregulated the expression of tumor necrosis factor (TNF)-α and reduced phosphorylation of inhibitor of kappa (Iκ) Bα induced by lipopolysaccharide in human embryonic kidney cells. Moreover, OEA downregulated the expression of interleukin (IL)-8 and IL-1β and inhibited the phosphorylation of IκBα and p65 induced by TNF-α in human enterocytes (Caco-2). The effect of OEA in reducing the expression of IL-8 was blocked by the peroxisome proliferator-activated receptor (PPAR)-α antagonist. During in vivo experiments on rats, colitis was induced by the oral administration of 8% dextran sulfate sodium from day 0 through day 5, and OEA (20 mg/kg) was intraperitoneally injected once a day from day 0 for 6 days. OEA administration significantly ameliorated the reduction in body weight, the increase in disease activity index score, and the shortening of colon length. In rectums, OEA administration reduced the infiltration of macrophages and neutrophils and tended to reduce the histological score and the expression of inflammatory cytokines. Administration of OEA produced significant improvement in a colitis model, possibly by inhibiting the nuclear factor kappa B signaling pathway through PPAR-α receptors. OEA could be a potential new treatment for IBD.
| S-EPMC7457075 | biostudies-literature
Project description:Ulcerative colitis (UC), with a long course and repeated attack, severely affects patient's life quality and increases economic burden all over the world. However, the concrete causes and mechanisms of UC are still unclear, but it is generally considered that many factors participate in this process. Qingchang Suppository (QCS) has been used in treating rectitis and colitis for about 30 years in Shanghai, China. Its satisfactory clinical effects have been proved. The aim of this study is to investigate the effect and mechanisms of QCS on colonic vascular endothelial barrier in dextran sulfate sodium (DSS)-induced colitis. The results indicated that increased vascular permeability (VP) appeared earlier than increased intestinal epithelial permeability (EP) in the process of DSS-induced colitis. QCS attenuated colonic tissue edema, vascular congestion and inflammatory cell infiltration. QCS inhibited the elevation of MPO, TNF-α, and IL-6 levels in colon tissues and alleviated the microvascular damage induced by DSS. QCS also improved colonic hypoxia and decreased the expression of VEGF, HIF-1α, and iNOS. These results revealed that QCS can reduce colonic VP and can improve vascular endothelial barrier function maybe by regulating the VEGF/HIF-1α signaling pathway.
| S-EPMC6220057 | biostudies-literature
Project description:AimsTo evaluate the effects of oligonol administration on experimentally induced colitis and colonic adenoma formation.ResultsOral administration of oligonol protected against mouse colitis induced by dextran sulfate sodium (DSS). Under the same experimental conditions, oligonol administration significantly inhibited the activation of nuclear factor-kappa B and signal transducer and activator of transcription (STAT) 3 and expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and cyclin D1 in the mouse colon. Further, oligonol inhibited azoxymethane-initiated and DSS-promoted adenoma formation in the mouse colon. Oligonol administration also attenuated lipid peroxidation (malondialdehyde) and protein oxidation (4-hydroxy-2-nonenal), thereby preventing oxidative stress-induced apoptosis of colonic epithelial cells. In vitro studies demonstrated that oligonol treatment reduced lipopolysaccharide-induced expression of interleukin (IL)-1β, tumor necrosis factor α, il-6, cox-2, and inos in murine macrophage RAW 264.7 cells. In another study, oligonol upregulated the antioxidant gene expression in the intestinal epithelial CCD841CoN cells and in the mouse colon.InnovationOligonol, an innovative formulation of catechin-type oligomers derived from the lychee fruit extract, was tested in this study for the first time to evaluate its effects on experimentally induced colitis and colonic adenoma formation in mice.ConclusionOligonol is effective in protecting against DSS-induced mouse colitis and colon carcinogenesis, suggesting that this polyphenol formulation may have a potential for the amelioration of inflammatory bowel disease and related disorders.
| S-EPMC3689162 | biostudies-literature