Distal Portions Of Small Intestine Research Articles

Validation of suitable reference genes for quantitative expression analysis by qPCR in bovine terminal ileum and ileocecal valve.

The use of reference genes is commonly accepted as the most reliable approach to normalize qRT-PCR and to reduce possible errors in the quantification of gene expression. The aim of this study was to identify a set of reference genes suitable for gene expression analysis in the distal portion of small intestine and ileocecal valve in cattle. These sites of intestine are of interest in veterinary science as they are the main sites of inflammation caused by Mycobacterium avium subsp. paratuberculosis, agent of paratuberculosis. We employed ten PCR assays for commonly used reference genes belonging to various functional classes and then determined their expression stability. The most stable genes were RPL13A and HMBS, followed by TFRC and B-ACT. NormFinder analysis provided similar results with B-ACT as the best reference gene, followed by RLP13A and TFRC. This validated gene panel may be useful for studies on paratuberculosis aiming to identify genes differentially expressed by qRT-PCR.

Abstract 5457: Chlorinated drinking water alters carcinogenesis in a mice model of colon cancer

Abstract Purpose: The gastrointestinal tract is constantly exposed to vast numbers of commensal bacteria and inflammatory product. The diet and enteric environment has been implicated in the pathogenesis of enterocolitis and colon cancer. Probiotic Lactbacilli modify the enteric microflora and are thought to have a beneficial effect on enterocolitis, eventually on colon cancer. We conducted this study to evaluate the effects of chlorinated drinking water which was used in general institutions. Experimental design: Mouse stains carrying colon epithelium-preferential Apc mutation (CPC;Apc mice), that show sporadic colorectal adenomas and carcinomas are used in this study. Nine of Eighteen CPC;Apc mice were consumed chlorinated drinking water (chlorinate concentrations of 10.0 mg/L) and 9 consumed tap water (chlorinate concentrations of 0.7 mg/L) for 25 week. Body weight was measured weekly. Faecal microbial analysis was performed. At sacrifice, the small and large bowel were histologically assessed. Results: Chlorinated drinking water strongly prevented intestinal tumorigenesis in terms of polyps formation in distal portion of small intestine. However, in colon we observed an increase in numbers and volumes of tumors. Body weight gain was more favorable by chlorine treated. Conclusions: These results show for the first time the efficacy and associated mechanisms of chlorinated drinking water feeding against spontaneous intestinal tumorigenesis in the CPC;Apc mice suggesting its chemopreventive potential against intestinal cancers. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5457. doi:1538-7445.AM2012-5457

Inhibition of intestinal adenoma formation in APC(Min/+) mice by Riccardin D, a natural product derived from liverwort plant Dumortiera hirsuta.

BackgroundMutation of tumor suppressor gene, adenomatous polyposis coli (APC), is the primary molecular event in the development of most intestinal carcinomas. Animal model with APC gene mutation is an effective tool for study of preventive approaches against intestinal carcinomas. We aimed to evaluate the effect of Riccardin D, a macrocyclic bisbibenzyl compound, as a chemopreventive agent against intestinal adenoma formation in APCMin/+ mice.Methods APCMin/+ mice were given Riccardin D by p.o. gavage for 7 weeks. Mice were sacrificed, and the number, size and histopathology of intestinal polyps were examined under a microscope. We performed immunohistochemical staining, western blotting, reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) in intestinal polyps to investigate the mechanism of chemopreventive effect of Riccardin D.ResultsRiccardin D treatment resulted in a significant inhibition of intestinal adenoma formation, showing a reduction of polyp number by 41.7%, 31.1% and 44.4%, respectively, in proximal, middle and distal portions of small intestine. The activity of Riccardin D against polyp formation was more profound in colon, wherein Riccardin D decreased polyp number by 79.3%. Size distribution analysis revealed a significant reduction in large-size polyps (2–3 mm) by 40.0%, 42.5% and 33.3%, respectively, in proximal, middle and distal portions of small intestine, and 77.8% in colon. Histopathological analysis of the intestinal polyps revealed mostly hyperplastic morphology without obvious dysplasia in Riccardin D-treated mice. Molecular analyses of the polyps suggested that the inhibitory effect of Riccardin D on intestinal adenoma formation was associated with its abilities of reduction in cell proliferation, induction of apoptosis, antiangiogenesis, inhibition of the Wnt signaling pathway and suppression of inflammatory mediators in polyps.ConclusionsOur results suggested that Riccardin D exerts its chemopreventive effect against intestinal adenoma formation through multiple mechanisms including anti-proliferative, apoptotic, anti-angiogenic and anti-inflammatory activity.

Chemoprevention of Intestinal Tumorigenesis in APCmin/+ Mice by Silibinin

Chemoprevention is a practical and translational approach to reduce the risk of various cancers including colorectal cancer (CRC), which is a major cause of cancer-related deaths in the United States. Accordingly, here we assessed chemopreventive efficacy and associated mechanisms of long-term silibinin feeding on spontaneous intestinal tumorigenesis in the APC(min/+) mice model. Six-week-old APC(min/+) mice were p.o. fed with vehicle control (0.5% carboxymethyl cellulose and 0.025% Tween 20 in distilled water) or 750 mg silibinin/kg body weight in vehicle for 5 d/wk for 13 weeks and then sacrificed. Silibinin feeding strongly prevented intestinal tumorigenesis in terms of polyp formation in proximal, middle, and distal portions of small intestine by 27% (P < 0.001), 34% (P < 0.001), and 49% (P < 0.001), respectively. In colon, we observed 55% (P < 0.01) reduction in number of polyps by silibinin treatment. In size distribution analysis, silibinin showed significant decrease in large-size polyps (>3 mm) by 66% (P < 0.01) and 88% (P < 0.001) in middle and distal portions of small intestine, respectively. More importantly, silibinin caused a complete suppression in >3 mm sized polyps and 92% reduction in >2 to 3 mm sized polyps in colon. Molecular analyses of polyps suggested that silibinin exerts its chemopreventive efficacy by inhibiting cell proliferation, inflammation, and angiogenesis; inducing apoptosis; decreasing beta-catenin levels and transcriptional activity; and modulating the expression profile of cytokines. These results show for the first time the efficacy and associated mechanisms of long-term p.o. silibinin feeding against spontaneous intestinal tumorigenesis in the APC(min/+) mice model, suggesting its chemopreventive potential against intestinal cancers including CRC.

Desenvolvimento e distribuição de Rodentolepis nana em Meriones unguiculatus

Com o objetivo de avaliar o desenvolvimento e a distribuição de Rodentolepis nana em Meriones unguiculatus, vinte animais receberam um inóculo oral de 100 ovos do parasito. A metade desses roedores recebeu, por via subcutânea, inóculo diário de dexametasona (DMS) (10mg/Kg). Aos 7 e 15 dias após a infecção (DPI), cinco animais de cada grupo foram sacrificados para a recuperação dos parasitos. Em M. unguiculatus não tratados, foram recuperados parasitos somente no 7o DPI, em início de maturação e distribuídos principalmente pela porção distal do intestino delgado desse roedor. Nesta mesma data, os parasitos recuperados em M. unguiculatus, que receberam DMS, estavam possivelmente no mesmo estádio que os encontrados em M. unguiculatus não tratados, porém distribuídos pelas porções média e distal do intestino delgado. Aos 15 DPI, os helmintos recuperados em M. unguiculatus que receberam DMS estavam completamente desenvolvidos, apresentando proglotes maduras e grávidas, distribuídos principalmente pela porção média, e, secundariamente, pela porção distal do intestino delgado. Conclui-se que M. unguiculatus tem reduzido potencial como reservatório deste cestóide e sua resistência à infecção pelo R. nana tem um importante componente inflamatório, sensível à ação da DMS.

Immunocytochemical localization of rat intestinal 15 kDa protein, a member of cytoplasmic fatty acid-binding proteins.

Rat intestinal 15 kDa protein (I-15P) is a member of the family of cytoplasmic fatty acid-binding proteins. Using a specific antiserum against I-15P, we studied the tissue distribution and subcellular localization of this protein in the entire rat body. By immunoblot analysis of cytosolic proteins, I-15P was detected not only in the distal portion of small intestine but also in the ovary and adrenal gland. Immunohistochemically, I-15P was localized to the absorptive epithelial cells as well as a subpopulation of enterochromaffin cells in the intestine, the lutein cells in the ovary, and subpopulations of cortical cells in the adrenal gland. Furthermore, I-15P-like immunoreactivity was also demonstrated in the surface mucous cells of stomach and the granular convoluted tubule cells of submandibular gland. Immuno-electron microscopy showed that the immunoreactivity was confined to the cytoplasmic matrix region, except in the enterochromaffin cells and granular convoluted tubule cells, where it was localized in the secretory granules. The present findings suggest that I-15P plays a role in the cellular metabolism of steroids.