Abstract | OBJECTIVE: METHODS:
Colitis was induced by intra- rectal administration of TNBS or DNBS. After TNBS/ DNBS injury, rats were treated with 10.0, 3.0, 1.0 or 0.3 mg/kg of Ro 48-5695 orally, daily for 5 days. On day 6 post- hapten treatment, colonic tissues were removed and examined in a blinded fashion for macroscopic damage (damage score) and myeloperoxidase (MPO) activity. Stool consistency and adhesions were also measured. RESULTS:
Oral administration of Ro 48-5695 almost completely prevented TNBS-induced damage at a dose of 10 mg/kg. The same dose in this model also had a therapeutic effect as measured by MPO and incidence of diarrhoea and adhesions. In DNBS-induced colonic damage, Ro 48-5695 was more potent and at 1.0 and 3.0 mg/kg decreased the damage score by 50 and 60% respectively; also the incidence of adhesions and diarrhoea was significantly reduced. However, MPO activity in this model was affected only by the highest dose of Ro 48-5695 tested (3.0 mg/kg) where it was reduced by 48%. CONCLUSIONS:
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Authors | I Padol, J Q Huang, C M Hogaboam, R H Hunt |
Journal | European journal of gastroenterology & hepatology
(Eur J Gastroenterol Hepatol)
Vol. 12
Issue 3
Pg. 257-65
(Mar 2000)
ISSN: 0954-691X [Print] England |
PMID | 10750644
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Benzenesulfonates
- Endothelin Receptor Antagonists
- Endothelin-1
- Ro 48-5695
- Sulfonamides
- dinitrobenzenesulfonic acid
- Trinitrobenzenesulfonic Acid
- Peroxidase
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Topics |
- Animals
- Benzenesulfonates
- Colitis, Ulcerative
(chemically induced, etiology, therapy)
- Disease Models, Animal
- Endothelin Receptor Antagonists
- Endothelin-1
(physiology)
- Inflammatory Bowel Diseases
(chemically induced, etiology, therapy)
- Male
- Peroxidase
(metabolism)
- Rats
- Rats, Sprague-Dawley
- Sulfonamides
(therapeutic use)
- Trinitrobenzenesulfonic Acid
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