New Ulcerative Colitis Model Induced by Sulfhydryl Blockers in Rats and the Effects of Antiinflammatory Drugs on the Colitis.

Satoh, Hiroshi; Sato, Fumihiko; Takami, Kenji; Szabó, Sándor

doi:10.1254/jjp.73.299

Cited by 41 publications

(34 citation statements)

References 33 publications

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“…In our study, we easily visualized extravasations of Evans blue as early as 1-2 days after DSS ingestion or 30 min to 12 h after IA enema as shown in Figure 1a, and blue color was strictly restricted to distal colon where DSS- 42 and IA-induced 13,14 lesions develop. Edema of the mucosal lamina propria and infiltration by inflammatory cells are constant features of human UC, reflecting increased VP providing thus direct human relevance of our experimental studies.…”

Section: Endothelial Damage In Ulcerative Colitismentioning

confidence: 56%

“…13,14 This model is characterized by welldefined time-dependent changes in colon, for example, depletion of antioxidant glutathione, increased alkylation of protein SH followed by the development of erosions, ulcers, and infiltration of neutrophils as early as 6-12 h after administration of the chemical. 13,14 This feature allowed us to detect very early changes, which precede the development of extensive colonic injury. Briefly, 0.1 ml of 6% IA (Sigma, St Louis, MO, USA) dissolved in 1% methylcellulose (Sigma) or the vehicle 1% methylcellulose was given to rats once by enema (7 cm from anus) via rubber catheter Nelaton S-8 (Rüsch, Germany).…”

Section: Iodoacetamide-induced Colitismentioning

confidence: 99%

“…Total proteins (100 mg), which were extracted from colonic mucosa in a lysis buffer containing protease inhibitors (Sigma), were processed routinely for western blotting as described previously. 14 The primary antibodies were used against Egr-1 (1:500; Santa Cruz Biotech, Santa Cruz, CA, USA) and HIF-1a (1:200, Novus Biologicals, LLC; Littleton, CO, USA). The loading controls were obtained by using antibody to b-actin (1:500; Santa Cruz Biotech).…”

Section: Western Blottingmentioning

confidence: 99%

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Early endothelial damage and increased colonic vascular permeability in the development of experimental ulcerative colitis in rats and mice

Tolstanova

Deng

French

et al. 2012

Laboratory Investigation

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The role of endothelial damage and increased vascular permeability (VP) in the pathogenesis of ulcerative colitis (UC) has not been investigated. We examined using functional, morphologic, and molecular biologic studies whether and to what extent the endothelial barrier dysfunction precedes enhanced epithelial permeability (EP) and the development of mucosal lesions during the early stages of experimental UC. We showed that in rats with iodoacetamide (IA)-induced UC increased colonic VP occurs early (ie, 2.6-fold increase at 15 min, Po0.01) preceding changes in epithelial barrier permeability. EP was unchanged at 15 and 30 min after IA administration and was increased 1.9-fold at 1 h and 6.7-fold at 2 h (both Po0.001) after IA. In the dextran sodium sulfate-induced slowly developing UC, colonic VP was significantly increased in 2 days (Po0.05) and EP only in 4 days (Po0.05). Mucosal endothelial injury led to hypoxia (Po0.05) of colonic surface epithelial cells 30 min after IA administration that was associated with increased expressions of transcription factors hypoxia-inducible factor-1a and early growth response-1. Electron and light microscopy demonstrated areas of colonic mucosa with perivascular edema covered by intact layer of surface epithelial cells in both rat and mouse models of UC. This is the first demonstration in four models of UC that endothelial damage, increased colonic VP, perivascular edema, and epithelial hypoxia precede epithelial barrier dysfunction that is followed by erosions, ulceration, and inflammation in UC. KEYWORDS: endothelial damage; epithelial permeability; hypoxia; inflammatory bowel disease; ulcerative colitis; vascular permeability Ulcerative colitis (UC) is characterized by chronic, recurrent ulcers and inflammation of the colonic mucosa. It has been postulated that impaired epithelial barrier function, resulting in penetration of bacteria and other antigens into the mucosa, is one of the major factors of UC pathogenesis.

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Section: Endothelial Damage In Ulcerative Colitismentioning

confidence: 56%

Section: Iodoacetamide-induced Colitismentioning

confidence: 99%

Section: Western Blottingmentioning

confidence: 99%

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Early endothelial damage and increased colonic vascular permeability in the development of experimental ulcerative colitis in rats and mice

Tolstanova

Deng

French

et al. 2012

Laboratory Investigation

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“…Therefore, more studies are required to further develop this area of research. The iodoacetamide-induced acute UC model in rat developed by Satoh et al [16] has been extensively studied [17,18] . In this model, an array of morphological and functional alterations have been described, however, the model lacked features of chronicity [17][18][19][20] .…”

Section: Introductionmentioning

confidence: 99%

Inflammatory bowel disease in rats: Bacterial and chemical interaction

Hussein¹,

Tohme²,

Barada³

et al. 2008

WJG

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“…Rats were weighed 9 AM to 10 AM before TNB administration as well as before necropsy. Diarrhea was graded according to the criteria: 0 (normal) to 3 (severe) (Satoh et al, 1997).…”

Section: Gross Observationmentioning

confidence: 99%

Intrarectal Dehydroleucodine Suppresses Trinitrobenzene Sulfonic Acid–Induced Colitis in Rats, A Model for Inflammatory Bowel Disease

Wendel¹,

María²,

Domínguez³

et al. 2007

Pharmaceutical Biology

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Dehydroleucodine (DhL), isolated from Artemisia douglasiana Besser (Asteraceae), prevents damage in acetic acid-induced colitis in rats. The trinitrobenzene sulfonic acid (TNBS)-induced model of chronic inflammation of the rat colon was used to determine the efficacy of DhL, at dose of 40 mg=kg, administered in enema form. All rats were sacrificed on day 7 and the colon excised, weighed, and rated macroscopically. Sections of colon were processed for light microscopy. Macroscopic scoring showed a decrease (p < 0.001) in the degree of damage in the DhL group compared with the group of rats treated with TNBS. Colon mass decreased (p < 0.05) in the DhL group compared with the TNBS group. Treatment with DhL resulted in a reduction in the incidence of diarrhea. Light-microscopic examination revealed preservation of mucosal architecture in the DhL-treated rats. DhL had an effective healing capacity at both macroscopic and microscopic levels. We conclude that DhL decreases injury and=or promotes healing in this model.

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New Ulcerative Colitis Model Induced by Sulfhydryl Blockers in Rats and the Effects of Antiinflammatory Drugs on the Colitis.

Cited by 41 publications

References 33 publications

Early endothelial damage and increased colonic vascular permeability in the development of experimental ulcerative colitis in rats and mice

Early endothelial damage and increased colonic vascular permeability in the development of experimental ulcerative colitis in rats and mice

Inflammatory bowel disease in rats: Bacterial and chemical interaction

Intrarectal Dehydroleucodine Suppresses Trinitrobenzene Sulfonic Acid–Induced Colitis in Rats, A Model for Inflammatory Bowel Disease

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