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1
Content available remote

The role of PPAR gamma agonists - rosiglitazone and 15-deoxy-delta12,14-prostaglandin J2 in experimental cyclosporine a hepatotoxicity

100%
Sikora-Wiorkowska A., Smolen A., Czechowska G., Wiorkowski K., Korolczuk A.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 6
2

Experimental models of cyclosporine A nephrotoxicity

100%
Korolczuk A., Maciejewski M., Czechowska G., Celinski K., Korobowicz E.
Bulletin of the Veterinary Institute in Puławy
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2010
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tom 54
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nr 1
59-62
The aim of this study was to compare the most commonly-used experimental models and to assess the microscopic renal changes in different models of cyclosporine A (CsA) nephrotoxicity. Wistar male rats were divided into five groups, eight animals in each. CsA was given in doses of 15 mg/kg, 25 mg/kg, and 100 mg/kg, respectively. The blood was collected for creatinine, urea, and uric acid levels analysis in the serum and the kidneys were sampled for microscopic examination on the 11th and 29th d of the experiment. CsA induced nephrotoxicity was characterised by increased serum levels of creatinine, urea, and uric acid. Microscopic features of CsA nephrotoxicity in all CsA experimental groups were observed. We would recommend the use of low doses of CsA for approximately 28 d as the most relevant experimental procedure for achieving the features of chronic CsA nephrotoxicity.
3
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The role of peroxisome-proliferator-activating receptor gamma agonists: rosiglitazone and 15-deoxy-delta12,14-prostaglandin J2 in chronic experimental cyclosporine A-induced nephrotoxicity

86%
Korolczuk A., Maciejewski M., Smolen A., Dudka J., Czechowska G., Widelska I.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 6
4
Content available remote

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

86%
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.
5
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Comparison of the anti-inflammatory and therapeutic actions of PPAR-gamma agonists rosiglitazone and troglitazone in experimental colitis

86%
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
6
Content available remote

Comparison of anti-inflammatory properties of peroxisome proliferator-activated receptor gamma agonists rosiglitazone and troglitazone in prophylactic treatment of experimental colitis

86%
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
7
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Effects of treatment with melatonin and tryptophan on liver enzymes, parameters of fat metabolism and plasma levels of cytokines in patients with non-alcoholic fatty liver disease – 14 months follow up

86%
Celinski K., Konturek P. C., Slomka M., Cichoz-Lach H., Brzozowski T., Konturek S. J., Korolczuk A.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 1
8
Content available remote

Protective effects of melatonin against thioacetamide-induced liver fibrosis in rats

86%
Czechowska G., Celinski K., Korolczuk A., Wojcicka G., Dudka J., Bojarska A., Reiter R. J.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 4
9

Wplyw inhibitorow ukladu renina-angiotensyna na obraz morfologiczny trzustki w eksperymentalnym przewleklym zapaleniu tego narzadu

86%
Madro A., Czechowska G., Korolczuk A., Celinski K., Slomka M., Prozorow-Krol B., Korobowicz E.
Medycyna Weterynaryjna
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2008
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tom 64
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nr 01
97-100
Chronic pancreatitis (CP) is a progressive disease, in which the exocrine function of the gland is gradually lost and fibrosis develops due to repeated episodes of acute pancreatitis. The detection of the renin-angiotensin system (RAS) brings us closer to understanding the pathogenesis of CP. It has been observed that the use of RAS inhibitors reduces hepatic fibrosis. The aim of the study was to examine the effects of RAS inhibitors on fibrotic processes in the course of experimental chronic pancreatitis induced by dibutyltin dichloride (DD). Chronic pancreatitis was induced by administering dibutyltin dichloride to the femoral vein and, simultaneously, captopril, losartan and enalapril which were administered intraperitoneally. The rats were decapitated after 60 days and pancreas tissue was collected for histopathology examination. No pathological changes were observed in the control group. Rats treated by dibutyltin dichloride displayed features of focal inflammatory infiltration, ductal lumen dilatation, fibrosis in the periductal spaces and slight interstitial fibrosis. Animals treated by RAS inhibitor displayed less severe inflammatory changes and fibrosis - particularly those rats treated by enalapril. The findings suggest that enalapril most effectively inhibits inflammatory changes and fibrosis.
10
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RAS inhibitors decrease apoptosis of acinar cells and increase elimination of pancreatic stellate cells after in the course of experimental chronic pancreatitis induced by dibutyltin dichloride

86%
Madro A., Korolczuk A., Czechowska G., Celinski K., Slomka M., Prozorow-Krol B., Korobowicz E.
Journal of Physiology and Pharmacology. Supplement
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2008
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tom 59
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nr 2
Chronic pancreatitis (CP) is a progressive disease, in which the exocrine function of the gland is gradually lost and fibrosis develops due to repeated episodes of acute pancreatitis. The aim of the study was to investigate the effects of RAS inhibitors on the apoptosis of acinar cells and pancreatic stellate cells (PSCs) elimination in experimental CP induced by dibutyltin dichloride (DBTC). CP was induced by administration of DBTC to the femoral vein. Simultaneously captopril, losartan, enalapril and lisinopril were administered intraperitoneally. The rats were decapitated after 60 days and tissue of pancreas was collected. In rats treated by DBTC the features of inflammatory infiltration, ductal lumen dilatation, fibrosis were found. Strong reactivity with capsase2L and clusterin-ß antibodies was observed in areas of fibrosis. In animals treated with RAS inhibitors inflammatory changes and fibrosis were less severe. In groups of rats treated with DBTC and RAS inhibitors immunoreactivity of capsase2L and clusterin-ß was weak. Positive immunostaining against smooth muscle actine and desmin was observed in the elongated cells (PSC-s). This reaction was weak in groups of rat treated with DBTC and RAS inhibitors. Treatment of CP rats with RAS inhibitors alleviate apoptosis of pancreatic acinar cells and induces PSCs elimination.
11
Content available remote

The effect of the angiotensin II receptor, type 1 receptor antagonists, losartan and telmisartan, on thioacetamide-induced liver fibrosis in rats

72%
Czechowska G., Celinski K., Korolczuk A., Wojcicka G., Dudka J., Bojarska A., Madro A., Brzozowski T.
Journal of Physiology and Pharmacology
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2016
|
tom 67
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nr 4
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