Project description:Background & Aims: Dextran sulphate sodium (DSS) induced colitis in rats is one of the most widely used models of inflammatory bowel disease. Animal models can provide new insights into the pathogenesis of intestinal inflammation, which is still unknown. We have performed a genomic analysis of the DSS rat colitis including an acute and a recovery phase. Methods: Expression profile of 6 control rats were compared with colitic rats at day 1 every other day until day 23 after DSS treatment using the GeneChip Rat Genome 230 2.0 Array (Affymetrix). Functional and pathways analysis were made with the differentially expressed genes. Keywords: Time course and differentially expressed genes analysis
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.
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.
Project description:Transcription profiling by array of mouse male retinas to investigate IGF-I-induced chronic gliosis and retinal stress IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death.
Project description:This study looks at the effect of glycomacropeptide (GMP) treatment on rats with trinitrobenzene sulfuric acid (TNBS) induced colitis.<br><br> Female Wistar rats (175-225 g) were randomly assigned to three different groups. A control group C (n=3) that did not receive the TNBS challenge but 0.25 ml of phosphate buffered saline (PBS) intrarectally, and two groups (group T (n=3) and group GMP (n=5) that received the TNBS challenge as described below. Group GMP received 500 mg kg-1 day-1 of GMP in 1% methylcellulose p.o, starting two days before the TNBS challenge. Treatment was administered to rats for five days after the TNBS challenge using an oesophageal catheter. The T group received the vehicle. Colitis was induced by the method of Morris et al. with minor modifications (13). Briefly, animals were fasted overnight and anaesthetized with halothane. Under these conditions, animals were given 10 mg of TNBS dissolved in 0.25 ml of 50% ethanol (v v-1) by means of a Teflon cannula inserted 8 cm through the anus. Animals were kept in a head-down position for an additional 30 s and returned to their cage. Distal colon samples were obtained. For TNBS treated animals samples were obtained avoiding necrotic tissue.
Project description:Temporal genome profiling of DSS colitis The DSS induced mouse colitis model is often used to emulate Ulcerative Colitis (UC) in order understand pathophysiological mechanism of inflammatory bowel disease (IBD). Given the progressive nature of IBD, colon tissue gene expression changes during the evolution of disease, and knowing the changes in gene expression profiles could indentify potential diagnostic markers or additional therapeutic targets for colitis. Therefore, we performed temporal genome expression profiling analysis using the Affymetrix genome wide microarray system to identify broad scale changes in gene expression associated with the development of colitis. Keywords: Expression time course of mouse colon tissue induced by 3% DSS. C57BL/6J mice were given 3% DSS in the drinking water and tissues from individual cohorts were collected at days 0, 2, 4 and 6. Total RNA were extracted from the colon tissue and detected by Affymerix GeneChip Mouse Genome 430 2.0 Array.
Project description:The impact of the antiinflammatory agent 5-aminosalicylic acid (5-ASA) on the risk for colitis-associated colorectal cancer remains controversial. The chemopreventive activity of 5-ASA was evaluated in the Swiss Webster model of azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colitis-associated neoplasia. Mice were injected with AOM (7.4 mg/kg i.p.) and randomized to receive either vehicle or 5-ASA (75mg/kg) for the remainder of the study. Only untreated animals were used in this array. DSS treatment began at 9 weeks of age and continued for 3 cycles. At the time of sacrifice (18 weeks of age), the entire colon and rectum were processed for histopathologic examination and microarray profiling. For information regarding the histopathological analysis, refer to Clapper ML, Gary MA, Coudry RA, Litwin S, Chang WC, Devarajan K, Lubet RA, Cooper HS. 5-aminosalicylic acid inhibits colitis-associated colorectal dysplasias in the mouse model of azoxymethane/dextran sulfate sodium-induced colitis. Inflamm Bowel Dis. 2008 Oct;14(10):1341-7. doi: 10.1002/ibd.20489. PMID: 18452197.
Project description:Background & Aims: Dextran sulphate sodium (DSS) induced colitis in rats is one of the most widely used models of inflammatory bowel disease. Animal models can provide new insights into the pathogenesis of intestinal inflammation, which is still unknown. We have performed a genomic analysis of the DSS rat colitis including an acute and a recovery phase. Methods: Expression profile of 6 control rats were compared with colitic rats at day 1 every other day until day 23 after DSS treatment using the GeneChip Rat Genome 230 2.0 Array (Affymetrix). Functional and pathways analysis were made with the differentially expressed genes. Experiment Overall Design: Experimental design: DSS was administered to animals in drinking water as follows:5%DSS from day 1 to 7, 3%DSS from day 8 to 15, 0% DSS from day 16 to 23. Samples were recovered at days 1, 3, 5, 7 (5%DSS), 9, 11, 13, 15 (2%DSS), 17, 19, 21 and 23 (0%DSS). According to inflammatory markers (Myeloperoxidase activity activity, body weight loss, colonic weigth/length ratio), three replicates at each time point were selected for genomic analysis and 6 control healthy rats (42 arrays). Experiment Overall Design: RNA was extracted from homogenized full-thickness colonic tissues in Trizol® reagent (Invitrogen) and purified with RNeasy affinity columns (Qiagen), according to manufacturer´s protocol. The microarray analysis was performed by Progenika Biopharma (Bilbao, Spain) on GeneChip® Rat Genome 230 2.0 Array (Affymetrix). All sample labeling (biotin), hybridization, staining and scanning procedures were carried out using Affimetrix, standard protocols (www.affymetrix.com). Normalization was carried out using Bioconductor sofware (affyPLM package).