Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA102933 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genomic profile of dextran sulphate sodium-induced colitis model in rats
| PRJNA102915 | ENA
Project description:Trinitrobenzenesulfonic acid (TNBS) rat colitis is one of the most widely used models of inflammatory bowel disease, a condition whose etiology and pathophysiology are incompletely understood. We have characterized the model at the genomic level following a longitudinal approach. Keywords: Time course and differentially expressed genes analysis
2008-11-01 | GSE9293 | GEO
Project description:Inflammatory bowel disease is a chronic colonic inflammation that displays symptoms like diarrhea and weight loss. Acupuncture has been widely accepted by Western countries for the treatment of pain. In this study, we analyzed the efficacy and mechanism of electroacupuncture (EA) on trinitrobenzene sulphonic acid (TNBS)-induced colitis in mice. Mice were intrarectally administered 250 mg/kg TNBS and electroacupunctured at Quze (PC3) and Neiguan (PC6) acupoints, which have been applied for gastrointestinal disorders. Gene expression profiles in colons and spleens were analyzed by microarray for the elucidation of mechanism of EA. Our data showed that EA at PC3 and PC6 improved macroscopic and microscopic features of colitis, and the improvement displayed a frequency-dependent manner. Administration of TNBS upregulated the expression of most cytokine genes in colons, while EA downregulated the expression of TNBS-induced cytokine genes. Pathway analysis showed that EA significantly affected inflammatory pathways in colons and immunity-associated pathway in spleens. Immunohistochemical staining further showed that EA decreased the expression of interleukin-1? and nuclear factor-?B. In conclusion, this is the first study reporting the global gene expression profiles of EA on TNBS-induced colitis. Our findings suggested that inflammatory and immunity pathways were involved in the anti-inflammatory mechanism of EA on colitis induced by TNBS. In this study, we analyzed the efficacy and mechanism of electroacupuncture (EA) on trinitrobenzene sulphonic acid (TNBS)-induced colitis in mice. Mice were intrarectally administered 250 mg/kg TNBS and electroacupunctured at Quze (PC3) and Neiguan (PC6) acupoints, which have been applied for gastrointestinal disorders. Gene expression profiles in colons and spleens were analyzed by microarray for the elucidation of mechanism of EA.
2014-09-02 | E-GEOD-57771 | biostudies-arrayexpress
Project description:We investigated the relationship between chronic inflammation and fibrosis in a mouse model of chronic colitis. Six weekly Trinitrobenzenesulphonic acid (TNBS) enemas were given to establish colitis and temporal changes in gene expression was elucidated over the next six weeks. Experiment Overall Design: After the six TNBS enemas, mice were sacrificed at 3 days (termed as TNBS-w6, n=6), 2 weeks (TNBS-w8, n=4), 4 weeks (TNBS-w10, n=5), or 6 weeks (TNBS-w12, n=4). The saline control groups were also sacrificed at week 6 (Saline-w6, n=5), week 8 (n=2) and week 10 (n=2). The last two sets were pooled as Saline-w10 (n=4). Two replicates of saline-w6 were analyzed. We compared Saline-w6 with TNBS-w6, and Saline-w10 with TNBS-w8, TNBS-w10, TNBS-w12, respectively.
2008-06-14 | E-GEOD-5864 | biostudies-arrayexpress
Project description:Experimentally induced colitis with trinitrobenzene sulphonic acid (TNBS) was used to generate models that are used to examine the pathogenesis of gut inflammation. TNBS-solution was rectally instilled in rats and development was observed by colonoscopy and genome wide transcription profiling.
2013-02-10 | E-MTAB-1263 | biostudies-arrayexpress
Project description:Ulcerative colitis (UC), a chronic, nonspecific inflammatory bowel disease characterized by continuous and diffuse inflammatory changes in the colonic mucosa, requires novel treatment method. Photodynamic therapy (PDT), as a promising physico-chemical treatment method, were used to treat UC rats’ model with novel photosensitizer LD4 in this paper, the treatment effect and mechanism was investigated. LD4-PDT could improve the survival rate of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced UC model rats, decrease expression of interleukin (IL)-6, IL-1, tumor necrosis factor (TNF)-α, malondialdehyde (MDA), myeloperoxidase (MPO) and increase the expression of glutathione (GSH) and superoxide oxidase (SOD), while protecting the integrity of the intestinal epithelium. LD4-PDT treatment could rebuild the intestinal microflora composition and reprogram the colonic protein profiles in TNBS-induced rats to almost the normal state. Proteomics analysis based upon TNBS-induced UC model rats revealed that Amine oxidase copper-containing 1 (AOC1) was a potential target of LD4-PDT. Novel photosensitizer agent LD4-PDT represents an efficient treatment method for UC, and AOC1 may be a promising target.
2021-09-24 | PXD027815 | Pride
Project description:Colitis is the common pathological lesion of inflammatory bowel diseases, the major chronic inflammatory diseases of intestinal tracts in humans. In this study, we investigated the therapeutic effects of ginger extract and its component zingerone in mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Mice were administered with TNBS and/or various amounts of ginger and zingerone by an intrarectal route. The severity of colitis was evaluated by colonic weight/length ratio, macroscopic lesion, and histological examination. The mechanisms of ginger and zingerone were further elucidated by DNA microarray, ex vivo imaging, and immunohistochemical staining. Our data showed that treatment with ginger extract and zingerone ameliorated TNBS-induced colonic inflammation and injury in a dose-dependent manner. Pathway analysis of ginger- and zingerone-regulated gene expression profiles showed that ginger and zingerone significantly regulated cytokine-related pathways. Network analysis showed that nuclear factor-κB (NF-κB) and interleukin-1β (IL-1β) were key molecules involved in the expression of ginger- and zingerone-affected genes. Ex vivo imaging and immunohistochemical staining further verified that ginger and zingerone suppressed TNBS-induced NF-κB activation and decreased the NF-κB and IL-1β protein levels in the colon. In conclusion, our data showed that ginger improved the TNBS-induced colitis in mice via modulation of NF-κB activity and IL-1β signaling pathway. Moreover, zingerone might be the active component of ginger responsible for the amelioration of colitis induced by TNBS. A total of 24 mice was randomly divided into four groups of six mice: mock, mice were given with 0.1 ml of 50% ethanol; TNBS, mice were given with 250 mg/kg TNBS in 0.1 ml of 50% ethanol; TNBS/ginger, mice were administered with mixtures containing 250 mg/kg TNBS and various amounts of ginger extract in 0.1 ml of 50% ethanol; TNBS/zingerone, mice were given with mixtures containing 250 mg/kg TNBS and various amounts of zingerone in 0.1 ml of 50% ethanol. Mice were sacrificed seven days later for histochemical staining, RNA extraction, and ex vivo imaging.
2015-04-28 | E-GEOD-37677 | biostudies-arrayexpress
Project description:Inflammatory bowel disease is a chronic colonic inflammation that displays symptoms like diarrhea and weight loss. Acupuncture has been widely accepted by Western countries for the treatment of pain. In this study, we analyzed the efficacy and mechanism of electroacupuncture (EA) on trinitrobenzene sulphonic acid (TNBS)-induced colitis in mice. Mice were intrarectally administered 250 mg/kg TNBS and electroacupunctured at Quze (PC3) and Neiguan (PC6) acupoints, which have been applied for gastrointestinal disorders. Gene expression profiles in colons and spleens were analyzed by microarray for the elucidation of mechanism of EA. Our data showed that EA at PC3 and PC6 improved macroscopic and microscopic features of colitis, and the improvement displayed a frequency-dependent manner. Administration of TNBS upregulated the expression of most cytokine genes in colons, while EA downregulated the expression of TNBS-induced cytokine genes. Pathway analysis showed that EA significantly affected inflammatory pathways in colons and immunity-associated pathway in spleens. Immunohistochemical staining further showed that EA decreased the expression of interleukin-1β and nuclear factor-κB. In conclusion, this is the first study reporting the global gene expression profiles of EA on TNBS-induced colitis. Our findings suggested that inflammatory and immunity pathways were involved in the anti-inflammatory mechanism of EA on colitis induced by TNBS.
2014-09-02 | GSE57771 | GEO
Project description:We investigated the relationship between chronic inflammation and fibrosis in a mouse model of chronic colitis. Six weekly Trinitrobenzenesulphonic acid (TNBS) enemas were given to establish colitis and temporal changes in gene expression was elucidated over the next six weeks. Keywords: disease state analysis
2007-12-10 | GSE5864 | GEO
Project description:Colitis is the common pathological lesion of inflammatory bowel diseases, the major chronic inflammatory diseases of intestinal tracts in humans. In this study, we investigated the therapeutic effects of ginger extract and its component zingerone in mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Mice were administered with TNBS and/or various amounts of ginger and zingerone by an intrarectal route. The severity of colitis was evaluated by colonic weight/length ratio, macroscopic lesion, and histological examination. The mechanisms of ginger and zingerone were further elucidated by DNA microarray, ex vivo imaging, and immunohistochemical staining. Our data showed that treatment with ginger extract and zingerone ameliorated TNBS-induced colonic inflammation and injury in a dose-dependent manner. Pathway analysis of ginger- and zingerone-regulated gene expression profiles showed that ginger and zingerone significantly regulated cytokine-related pathways. Network analysis showed that nuclear factor-κB (NF-κB) and interleukin-1β (IL-1β) were key molecules involved in the expression of ginger- and zingerone-affected genes. Ex vivo imaging and immunohistochemical staining further verified that ginger and zingerone suppressed TNBS-induced NF-κB activation and decreased the NF-κB and IL-1β protein levels in the colon. In conclusion, our data showed that ginger improved the TNBS-induced colitis in mice via modulation of NF-κB activity and IL-1β signaling pathway. Moreover, zingerone might be the active component of ginger responsible for the amelioration of colitis induced by TNBS.
2015-04-28 | GSE37677 | GEO