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  1. 27 Journal of Physiology and Pharmacology

  2. 2 Archivum Immunologiae et Therapiae Experimentalis

  3. 1 Acta Parasitologica

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  1. 6 Konturek P. C.

  2. 5 Brzozowski T.

  3. 4 Burnat G.

  4. 4 Konturek S. J.

  5. 4 Sliwowski Z.

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1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Activation of dendritic cells by nematode antigens during colitis

100%
Maruszewska-Cheruiyot M., Donskow-Lysoniewska K., Piechna K.
Annals of Parasitology
|
2016
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tom 62
|
nr Suppl.
2

Effect of iron supplementation on intestinal function and oxidative stress in piglets with induced colitis

86%
Chen Q., Le G. W., Shi Y. H., Zhang S. M., Jin X.
Journal of Animal and Feed Sciences
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2007
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tom 16
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nr 2
205-213
3
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Dual role of endogenous nitric oxide in development of dextran sulfate sodium-induced colitis in rats

86%
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.
4
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Prophylactic potential of montelukast against mild colitis induced by dextran sulphate sodium in rats

86%
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.
5
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Content available

Experimental inflammatory bowel disease - role of T cells

86%
Szczepanik M., Gryglewski A., Bryniarski K., Stachura J., Ptak W.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 2
6
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High activity of the endogenous opioid system and acute but not chronic stress influence experimental colitis development in mice

72%
Zielinska M., Szymaszkiewicz A., Salaga M., Zatorski H., Wlodarczyk J., Jacenik D., Kordek R., Krajewska W. M., Misicka A., Fichna J., Sacharczuk M.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 5
7
Content available remote

Evaluation of the effect of liposomes loaded with chlorogenic acid in treatment of 2,4,6-trinitrobenzenesulfonic acid-induced murine colitis

72%
Krajewska J. B., Pietruszka P., Tomczyk D., Chen C., Owczarek A., Karolewicz B., Czapor-Irzabek H., Gorniak A., Fichna J.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 2
8

The pathogenic role of Blastocystis isolated from patients with irritable bowel syndrome and colitis from Iasi, Romania

72%
Matiut D. S., Hritcu L.
Acta Parasitologica
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2015
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tom 60
|
nr 1
9
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Curcumin improves experimentally induced colitis in mice by regulating follicular helper T cells and follicular regulatory T cells by inhibiting interleukin-21

72%
Li S.-Q., Lv X.-D., Liu G.-F., Gu G.-L., Chen R.-Y., Chen L., Fan J.-H., Wang H.-Q., Liang Z.-L., Jin H., Qin L.-F., Xie Y.-F., Lu F., Jiang H.-X., Zhan L.-L., Lv X.-P.
Journal of Physiology and Pharmacology
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2021
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tom 72
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nr 1
10
Content available remote

Exploring novel colon-targeting antihistaminic prodrug for colitis

72%
Dhaneshwar S., Gautam H.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 4
11
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St. John's wort may ameliorate 2,4,6-trinitrobenzenesulfonic acid colitis of rats through the induction of pregnane X receptors and/or P-glycoproteins

72%
Sehirli A. O., Cetinel S., Ozkan N., Selman S., Tetik S., Yuksel M., Dulger F. G. A.
Journal of Physiology and Pharmacology
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2015
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tom 66
|
nr 2
12

Prostaglandins and inflammation: the cyclooxygenase controversy

72%
Morteau O.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
tom 48
|
nr 6 Spec.Iss.
473-480
13
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Mice lacking cannabinoid CB1-, CB2-receptors or both receptors show increased susceptibility to trinitrobenzene sulfonic acid [TNBS]-induced colitis

72%
Engel M. A., Kellermann C. A., Burnat G., Hahn E. G., Rau T., Konturek P. C.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 1
89-97
This study was performed to assess whether mice lacking the cannabinoid receptor CB1, CB2 or both receptors show increased susceptibility to TNBS colitis in comparison to wildtype mice. Previously, activation of CB1 and CB2 receptors showed attenuation of TNBS colitis in mice. The aim of the study was to investigate the susceptibility of three mouse strains CB1-, CB2- and CB1+2 double knockout mice in the model of TNBS colitis. The different knockout mice were given each a single enema with TNBS 7 mg, volume 150 µl (in 50% ethanol solution) on day 1. Control group (C57BL/6 mice) received the same concentration of TNBS enema and each strain received vehicle application of 150 µl 50% ethanol solution. After a 3-day period, the animals were sacrificed and their colon excised. A scoring system was used to describe macroscopical and histological changes. Messenger RNA-expression of TNF- and IL-1ß as pro-inflammatory markers was measured by RT-PCR. All three knockout strains showed increased susceptibility to TNBS colitis quantified by macroscopical and histological scoring systems and pro-inflammatory cytokine expression in comparison to the TNBS control group (wild type C57BL/6 animals). Mice lacking the CB1-, CB2-receptor or both receptors showed aggravation of inflammation in the model of TNBS colitis. Lacking of both cannabinoid receptors did not result in potentiation of colitis severity compared to lacking of each CB1 or CB2, respectively. These results suggest that the endocannabinoid system may have tonic inhibitory effects on inflammatory responses in the colon.
14
Content available remote

Anti-inflammatory effects of nesfatin-1 in rats with acetic acid - induced colitis and underlying mechanisms

72%
Ozturk C. C., Oktay S., Yuksel M., Akakin D., Yarat A., Kasimay Cakir O.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 5
15
Content available remote

Roles of nitric oxide (NO) and NO synthases in healing of dextran sulfate sodium-induced rat colitis

72%
Aoi Y., Terashima S., Ogura M., Nishio H., Kato S., Takeuchi K.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 2
We examined the effects of various NO inhibitors on the healing of DSS-induced rat colitis. Experimental colitis was induced by feeding rats for 6 days with 2.5% DSS in drinking water. After DSS treatment, the animals were fed normally and killed various days up to 7 days later. L-NAME (a nonselective NOS inhibitor) or aminoguanidine (a selective iNOS inhibitor) was given p.o. twice daily for 6 days starting from the termination of DSS treatment. The area of lesions, colon length and MPO activity were measured on day 7 after DSS treatment. DSS treatment caused severe lesions in the colon, accompanied by an increase in MPO activity and a decrease in colon length. The lesions healed gradually after discontinuation of DSS treatment, with a histological restoration and subsidence of inflammation. The healing of DSS-induced colonic lesions was significantly impaired by daily administration of L-NAME or aminoguanidine, the effects being all but equivalent between these drugs, and the effect of L-NAME was significantly reverted by the co-administration of L-arginine. The expression of nNOS protein was observed in the colonic mucosa with or without DSS treatment, while those of iNOS and eNOS were markedly upregulated after DSS treatment. Likewise, the expression of VEGF was also up-regulated in the colon following DSS treatment, and this response was suppressed by both L-NAME and aminoguanidine. These results suggest that endogenous NO produced by mainly iNOS and partly eNOS contributes to the healing of DSS-induced colonic lesions, through the upregulation of VEGF expression and enhancement of angiogenesis.
16
Content available remote

Influence of the peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonist, rosiglitazone and antagonist , biphenol-A-diglicydyl ether (BADGE) on the course of inflammation in the experimental model of colitis in rats

58%
Dworzanski T., Celinski K., Karolczuk A., Slomka M., Radej S., Czechowska G., Madro A., Cichoz-Lach H.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 6
17
Content available remote

Participation of the intestinal microbiota in the mechanism of beneficial effect of treatment with synbiotic Syngut on experimental colitis under stress conditions

58%
Konturek P. C., Konturek K., Brzozowski T., Wojcik D., Magierowski M., Targosz A., Krzysiek-Maczka G., Sliwowski Z., Strzalka M., Magierowska K., Szczyrk U., Kwiecien S., Ptak-Belowska A., Neurath M., Dieterich W., Wirtz S., Zopf Y.
Journal of Physiology and Pharmacology
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2020
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tom 71
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nr 3
18
Content available remote

Ghrelin ameliorates colonic inflammation. Role of nitric oxide and sensory nerves.

58%
Konturek P. C., Brzozowski T., Engel M., Burnat G., Gaca P., Kwiecien S., Pajdo R., Konturek S. J.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 2
41-47
Ghrelin is a novel growth hormone (GH)-releasing and orexigenic peptide with anti-inflammatory activities. However, the role of ghrelin in the colonic inflammation is still controversial. The aim of the present study was: 1) to examine the expression of ghrelin and TNF- mRNA in the inflamed colonic mucosa of patients with ulcerative colitis (UC), 2) to analyze the effect of treatment with exogenous ghrelin on the healing of trinitrobenze sulphonic acid (TNBS)-induced colitis in rats, and 3) to assess the effects of ghrelin treatment on mRNA expression for iNOS and protein expression for COX-2 and PPAR in intact colonic mucosa and in that with TNBS-induced colitis. Fifteen patients with UC and fifteen healthy controls were enrolled in this study. Expression of ghrelin and TNF- was assessed by semi-quantitative RT-PCR in the colonic mucosal biopsies from UC patients and healthy controls. In addition, the effect of exogenous ghrelin on healing of TNBS colitis was tested in rats without or with capsaicin-induced functional ablation of sensory nerves. Patients with UC showed a significant upregulation of mRNA for ghrelin and TNF- in colonic mucosa as compared to that observed in healthy controls. The expression of ghrelin correlated with the grade of inflammation and expression of TNF-. In rats the exogenous ghrelin administered daily at a dose of 20 µg/kg i.p. significantly accelerated the healing of TNBS colitis and this effect was accompanied by an increase in mRNA expression for iNOS and protein expression for COX-2 in the colonic mucosa. The protein expression for PPAR, which was down-regulated in rat colonic mucosa after exposure to TNBS as compared to that in intact colonic mucosa, was not significantly influenced by ghrelin treatment. We conclude that 1) patients with UC show an increased mucosal expression of mRNA for ghrelin in the colonic mucosa which could trigger protective response in inflamed colon; and 2) exogenous ghrelin accelerates healing of colonic lesions in animal model of ulcerative colitis via increased release of NO and PGE2 due to an increase in iNOS and COX-2 expression and stimulation of sensory neuropeptides such as CGRP released from sensory afferent endings.
19
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Dextran sulphfate sodium induces pan-gastroenteritis in rodents: implications for studies of colitis

58%
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
20
Content available remote

Effects of peroxisome proliferator-activated receptors-gamma ligands on dextran sodium sulphate-induced colitis in rats

58%
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.
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