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Quantitative phosphosproteomics revealed the mechanism of Cyanidin-3-O-glucoside ameliorating dextran sulfate sodium (DSS)-induced colitis

ABSTRACT: As the exact molecular mechanisms of ulcerative colitis are not fully understood. Cyanidin-3-O-glucoside (C3G) is a compound derived from the food black rice. We investigated whether C3G can ameliorate DSS-induced colitis by using relevant predictions and experiments.

ORGANISM(S): Mus Musculus

SUBMITTER: Cheng Hu

PROVIDER: PXD043592 | iProX | Thu Jul 06 00:00:00 BST 2023

REPOSITORIES: iProX

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Mechanisms research on Cyanidin-3-O-glucoside ameliorating dextran sulfate sodium (DSS)-induced colitis.

Project description:TMT proteomics for colonic mucosa in DSS-induced colitis mice with or without administrated Cyanidin-3-O-glucoside was used for discovery of differential expressed proteins.

2023-07-10 | PXD043662 |

Gene expression profile of ATF6a and ATF6b knockout mice with dextran sulfate sodium (DSS)-induced colitis

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Anatabine ameliorates intestinal inflammation and reduces the production of pro-inflammatory factors in a dextran sulfate sodium mouse model of colitis.

Project description:Objective: In this study, we aimed to evaluate the anti-inflammatory properties of nicotine and anatabine in a dextran sulfate sodium (DSS) mouse model of ulcerative colitis (UC). Methods: C57BL/6 male mice (10 groups with 8 animals each) were orally administered nicotine at a concentration of 5 or 20 mg/kg body weight or anatabine at a concentration of 5 or 20 mg/kg body weight for a total of 21 days. Colitis was induced by oral administration of 3.5% DSS in drinking water ad libitum during days 14–21. Colonic samples were collected for transcriptomic analysis and multi-analyte profiling (MAP). Results: Oral administration of anatabine, but not nicotine, reduced the clinical symptoms of DSS-induced colitis. The result of gene expression analysis suggested that anatabine had a restorative effect on global DSS-induced gene expression profiles, while nicotine only had limited effects. Accordingly, MAP findings revealed that anatabine reduced the colonic abundance of DSS-associated cytokines and increased IL‑10 abundance. Conclusions: Our results support the reduction of inflammatory effects by anatabine in the DSS mouse model of UC.

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Dextran sodium sulfate treatment of Pirc rats alters colonic and tumor gene expression

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Toll-like receptor 2 deficiency exacerbates dextran sulfate sodium (DSS)-induced intestinal injury by Marinifilaceae dependent attenuating cell cycle signaling

Project description:Ulcerative colitis (UC) is an intestinal pathology characterized by chronic recurrent inflammation, which requires in-depth exploration of its mechanisms. To investigate the biological effects of TLR2 on DSS-induced intestinal inflammation in mice, we constructed the WT and TLR2-KO colitis mice model. We found TLR2-KO mice were severely susceptible to DSS-induced colitis. To determine how TLR2 exerted a protective effect in DSS-induced colitis, we compared the global gene expression profiles in the gut between WT and TLR2-KO mice by RNA-Seq. Results suggested that cell cycle pathway-related genes were significantly downregulated in gut of TLR2-KO colitis mice. 16S rRNA gene sequencing demonstrated remarkable variation in the composition of gut microbiota between WT and TLR2-KO colitis mice. Compared with WT colitis mice, the relative abundance of Marinifilaceae, Rikenellaceae, Desulfovibrionaceae, Tannerellaceae, Ruminococcaceae, Clostridia, Mycoplasmataceae were significantly higher in the gut of TLR2-KO colitis mice at family level. Moreover, we found that the relative abundance of Marinifilaceae was negatively correlated with the expression of cell cycle signaling related genes by microbiome diversity-transcriptome collaboration analysis. We came to this conclusion: TLR 2-KO exacerbated DSS-induced intestinal injury by Marinifilaceae dependent attenuating cell cycle signaling.

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Dextran sodium sulfate treatment of wild type and Pirc rats alters colonic normal tissue gene expression

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2014-01-14 | E-GEOD-54005 | biostudies-arrayexpress

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Gene Array Analysis of Methylthioadenosine Supplementation in Dextran Sulfate Sodium Induced Colitis

Project description:Study hypothesized that oral supplementation of methylthioadenosine (MTA) would reduce the inflammatory response in mice exposed to an agent that induces colitis (DSS) and that this reduction in inflammatory response would lead to reduced clinical disease burden. Total RNA was collected from isolated colons of mice in the following treatment groups: untreated controls, DSS only, DSS+MTA

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M1002 protect mice from DSS-induced colitis through regulation of HIF-1 signaling and the Gut Microbiota in DSS-Induced Colitis in Mice

Project description:Abstract. Ulcerative colitis (UC) is an intestinal disease characterized by chronic recurrent inflammation, but the underlying mechanism remains undefined and requires in-depth exploration. The aim of the present study was to investigate the biological effects of a small molecular compound M1002 of oxygen-sensing signaling pathway on dextran sulfate sodium (DSS)-induced intestinal inflammation colitis mouse models. It was found that the protective effects of M1002 on DSS-induced colitis. To determine how M1002 exerted its protective effect in DSS-induced colitis, we compared the global gene expression profiles in the gut between DSS control and M1002 treatment colitis mouse groups by RNA-Seq. The results demonstrated that HIF-1 signaling pathway-related genes were significantly upregulated in the gut of M1002 treatment colitis mice, whereas the Inflammatory bowel disease signaling pathway, the TNF signaling pathway, and Cytokines and inflammatory response signaling pathway related genes were significantly downregulated in the M1002 treatment group. 16S rRNA gene sequencing demonstrated remarkable variations in the composition of gut microbiota between DSS control and M1002 treatment colitis mice. Compared with DSS control colitis mice, the relative abundance of Eubacterium_nodatum and Halomonas in the gut microbiota was significantly increased at genus level in the gut of M1002 treatment colitis mice. Based on these findings, we tend to conclude that M1002 might alleviate DSS-induced gut injury in mice by regulation of HIF-1 signaling and up-regulating Eubacterium_nodatum and Halomonas.

2025-07-01 | GSE271173 | GEO

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