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Abstract

Aim of this study was to assess the structural, ultrastructural, immunohistochemical, and clinical aspects in Sprague-Dawley rats with dextrane sulfate sodium (DSS)-induced colitis. Colitis was induced in Sprague-Dawley rats by seven days of DSS oral administration followed by seven days of tap water only (for one, two and three cycles). Controls were fed with water only. Segments of proximal, mid-, and distal colon of each animal were adequately prepared for light and scanning electron microscope observations. The severity of the lesions was scored histologically. For immunohistochemical study, a cocktail of S-100, NSE, and antineurofilament antibodies was used. Symptoms such as weight, feces consistency, diarrhea, hematochezia were recorded daily. From a clinical point of view symptoms appeared significantly later after the first cycle than after the second and third cycles and lasted significantly longer in the second and third cycles. Treated rats showed a slower weight gain rate by 20% compared to controls, and the whole colon length appeared to be significantly shorter after colitis induction compared to controls. Structural observations by light microscopy showed prominent involvement of the distal colon. Immunohistochemical study of both submucosal and myoenteric nerve plexuses was similar to controls. Scanning electron microscope observations of the colonic mucosal surface in colitis rats showed a complete subversion of its architecture, characterized by dilatations of gland crypt openings, dropout of goblet cells, and inhomogeneous distribution or lack of microvilli. These were most evident after the third cycle. In conclusion, experimental DSS colitis in SD rats appeared to be highly reproducible and shared most features with human UC, not only from a structural and clinical but also from an ultrastructural point of view.

Sodium arsenite reduces severity of dextran sulfate sodium-induced ulcerative colitis in rats

“…Most of these histological changes have been observed by others in several DSS colitis rat models (Gaudio et al, 1999;Iba et al, 2003;Herias et al, 2005). Peculiar to our study, we noted that the severity of these lesions increased with time so that the most severe lesions were observed in Cycle 3, less severe in Cycle 2, and the least severe in Cycle 1.…”

“…In several rat models of DSS colitis, diarrhea, loose stools, hemoccult positive stools, gross bleeding, and loss of body weight are common signs observed (Gaudio et al, 1999;Kullmann et al, 2001;Vetuschi et al, 2002;Iba et al, 2003). They can occur as early as Day 2 in acute colitis rat models and as Day 4 in chronic models (Kullmann et al, 2001).…”

“…Advances in research have identified the interaction between genetic, infectious, immunological and environmental factors to play role in their pathogenesis (Gaudio et al, 1999;Vetuschi et al, 2002). Although their exact cause remains unclear, immunological dysfunction seems to initiate a self-sustaining inflammatory process (Podolsky, 1991) manifested by elevated levels of the chemoattractant interleukin (IL)-8 that is responsible for the attraction and infiltration of neutrophils to the colon mucosa and the subsequent pathology.…”

Effects of Proteoglycan on Dextran Sulfate Sodium-Induced Experimental Colitis in Rats

“…We suggest that the anti-inflammatory effect of PG on DSS- induced colitis may be due to the increase of n-butyrate and that for this role the structure of PG is important. DSS-induced experimental colitis resembles human UC [12], is reproducible, and seems to be an adequate model for verifying the efficacy of drugs in preventing or healing colitis lesions [19,20]. Overgrowth of Bacteroides and Clostridium species has been demonstrated [12], and a topical toxic effect of DSS on colonic epithelial cells has also been proposed [21].…”

“…Therefore, we examined inflammatory cell infiltration in the most severe lesions (erosive area). In acute DSS colitis, the inflammatory infiltrate in the erosive area consists of neutrophils, lymphocytes, and plasma cells [12,15,19]. Oral administration of PG significantly reduced neutrophil infiltration into the lamina propria mucosae and submucosa in the areas of erosion induced by DSS (Fig.…”