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1
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Dual role of endogenous nitric oxide in development of dextran sulfate sodium-induced colitis in rats

100%
Rumi G., Tsubouchi R., Nishio H., Kato S., Mozsik G., Takeuchi K.
Journal of Physiology and Pharmacology
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2004
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tom 55
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nr 4
The role of nitric oxide (NO) in the etiology of ulcerative colitis is controversial with reports of the improvement and aggravation of colonic lesions by inducible NO synthase (iNOS) inhibitors. In the present study, we compared the effect of the selective iNOS inhibitor aminoguanidine and the nonselective NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on a dextran sulfate sodium (DSS)-induced model of colitis in rats. Experimental colitis was induced by a 3% DSS-solution added to drinking water for 7 days. Aminoguanidine (5~20 mg/kg) and L-NAME (10 mg/kg) were administered p.o. twice daily for the first 3 days, the last 3 days or all 6 days of DSS treatment. Body weight and severity of colitis (diarrhea, bloody feces) were observed over a period of 7 days. DSS treatment resulted in severe colonic lesions, accompanied by diarrhea, bloody feces, decrease of body weight and colon shortening. All of the parameters investigated improved significantly with aminoguanidine treatment at 20 mg/kg for 6 days or the last 3 days of DSS-treatment, but L-NAME did not significantly affect the colitis during these periods. When L-NAME or aminoguanidine was given in the first 3 days of DSS treatment, the colonic lesions were slightly aggravated by L-NAME but not affected by aminoguanidine. The expression of iNOS mRNA was observed from the 3rd day of DSS treatment. These results suggested that endogenous NO exerts a biphasic influence on DSS-induced colitis, depending on the NOS isoenzyme; a beneficial effect of NO derived from constitutive NOS and a detrimental effect of NO produced by iNOS in the development of colitis.
2
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Prophylactic potential of montelukast against mild colitis induced by dextran sulphate sodium in rats

100%
Holma R., Salmenpera P., Virtanen I., Vapaatalo H., Korpela R.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 3
Cysteinyl leukotrienes play a part in inflammatory processes such as inflammatory bowel diseases. The present study aimed to evaluate the effects of the cys-LT-1 receptor antagonist montelukast on a mild colitis model in rats. Colitis was induced by administrating 4% dextran sulphate sodium (DSS, MW 45 000) in drinking water for 9 days. Montelukast (10 mg/kg/day) or vehicle was given by gastric gavage once daily simultaneously with DSS administration. A healthy control group receiving water as drinking fluid and vehicle by gastric gavage was included. Body weight loss, consistency of faeces (loose/diarrhoea) and occult blood in the faeces/ gross bleeding were assessed on days 6 - 9. After sacrifice, the following were assessed: colonic histology, the expression of inducible nitric oxide synthase, macrophage/monocyte marker ED1, cyclooxygenase-1 and cyclooxygenase-2, as well as the production of leukotriene B4 and E4, prostaglandin E2, its metabolite bicyclic-prostaglandin E2 and thromboxane B2 in the colonic tissue incubation in vitro. Rats receiving DSS exhibited bloody diarrhoea from day 6 onwards. Montelukast significantly reduced the occult blood in the faeces/ gross bleeding, maintained normal body weight gain and tended to decrease the ratio of leukotriene B4/ prostaglandin E2 production in the colon in vitro. The results indicate that montelukast has some potential to ameliorate mild experimental colitis induced by DSS.
3
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Comparison of anti-inflammatory properties of peroxisome proliferator-activated receptor gamma agonists rosiglitazone and troglitazone in prophylactic treatment of experimental colitis

84%
Celinski K., Dworzanski T., Fornal R., Korolczuk A., Madro A., Brzozowski T., Slomka M.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 5
4
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Dextran sulphfate sodium induces pan-gastroenteritis in rodents: implications for studies of colitis

67%
Elsheikh W., Flannigan K. L., McKnight W., Ferraz J. G. P., Wallace J. L.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 5
5
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Effects of peroxisome proliferator-activated receptors-gamma ligands on dextran sodium sulphate-induced colitis in rats

67%
Celinski K., Dworzanski T., Korolczuk A., Piasecki R., Slomka M., Madro A., Fornal R.
Journal of Physiology and Pharmacology
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2011
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tom 62
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nr 3
Recent studies indicate the involvement of peroxisone proliferator-activated receptor- (PPAR-) in the inflammatory reaction. The exact mechanism of PPAR- action has not been elucidated. It is supposed that PPAR- regulates transcription of genes responsible for encoding cytokines involved in the inflammatory response. The latest studies, carried out to explain the pathogenesis of non-specific colitis, confirm beneficial effects of PPAR- agonists on attenuation of colon inflammation. The aim of the present study was to assess the effects of nuclear PPAR- activity on the course of experimental acute colitis induced by intragastric administration of dextran sodium sulphate (DSS) using the PPAR- agonist rosiglitazone and the antagonist BADGE in rats. Colitis in Wistar rats was induced by 1.5% DSS administered in drinking water for 8 days. Animals with induced colitis received rosiglitazone, bisphenol A diglycidyl ether (BADGE) or both substances. After decapitation, colons were macroscopically and histopathologically evaluated. Levels of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor- (TNF-) and myeloperoxidase (MPO) were determined in serum and colon homogenates using ELISA. In rats with experimentally induced colitis receiving rosiglitazone, the inflammatory reaction was found to be markedly limited; ulceration, oedema and infiltration activity were reduced. The activated PPAR- inhibit the expression of proinflammatory factors, such as IL-6, TNF-, and neutrophil chemotaxis, which was evidenced by MPO reduction in serum and colon homogenates mediated by rosiglitazone. The positive effects of rosiglitazone on expression of IL-10 were also demonstrated. During the short period of observation, BADGE did not increase histopathological inflammatory markers.
6
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Comparison of the anti-inflammatory and therapeutic actions of PPAR-gamma agonists rosiglitazone and troglitazone in experimental colitis

67%
Celinski K., Dworzanski T., Fornal R., Korolczuk A., Madro A., Slomka M.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 6
7

Oral in vivo bactofection in dextran sulfate sodium treated female Wistar rats

67%
Palffy R., Behuliak M., Gardlik R., Jani P., Kadasi L., Turna J., Celec P.
Folia Biologica
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2010
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tom 58
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nr 3-4
171-176
8
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Host nuclear factor erythroid 2-related factor 2 defense system determines the outcome of dextran sulfate sodium - induced colitis in mice

67%
Lee J. S., An J. M., Kang E. A., Han Y. M., Kim Y. S., Lee H. J., Kim K.-J., Surh Y. J., Hahm K.-B.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 5
9
Content available remote

Beneficial anti-inflammatory effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker in the treatment of dextran sulfate sodium-induced colitis in mice

67%
Salmenkari H., Pasanen L., Linden J., Korpela R., Vapaatalo H.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 4
10
Content available remote

Orally administered angiotensin-converting enzyme-inhibitors captopril and isoleucine-proline-proline have distinct effects on local renin-angiotensin system and corticosterone synthesis in dextran sodium sulfate-induced colitis in mice

67%
Salmenkari H., Holappa M., Forsgard R. A., Korpela R., Vapaatalo H.
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 3
11

Gut microbiota, probiotics and inflammatory bowel disease

59%
Stephani J., Radulovic K., Niess J. H.
Archivum Immunologiae et Therapiae Experimentalis
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2011
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tom 59
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nr 3
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