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1

Adiponektyna i adipsyna jako parametry przydatne w ocenie zaburzeń metabolicznych w cukrzycy typu 2

100%
Mizgala E., Mertas A., Szliszka E.
Diagnostyka Laboratoryjna
|
2017
|
tom 53
|
nr 1A
2

TRAIL-induced apoptosis and expression of death receptor TRAIL-R1 and TRAIL-R2 in bladder cancer cells

88%
Szliszka E., Mazur B., Zydowicz G., Czuba Z. P., Krol W.
Folia Histochemica et Cytobiologica
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2009
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tom 47
|
nr 4
3
Content available remote

Influence of 5-aminoisoquinolin-1-one (5-AIQ) on neutrophil chemiluminescence in rats with transient and prolonged focal cerebral ischaemia and after reperfusion

76%
Hendryk S., Czuba Z. P., Jedrzejowska-Szypulka H., Szliszka E., Phillips V. A., Threadgill M. D., Krol W.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 4
811-822
Stimulation of neutrophils by different factors increases their oxidative activity and the free radicals produced can report on the degree of activation. Poly(adenosine 5’-diphosphate ribose)polymerase-1 (PARP-1), a nuclear enzyme activated by strand breaks in DNA, plays an important role in the tissue injury associated with ischaemia-reperfusion injury and inflammation. 5-Aminoisoquinolin-1-one (5-AIQ) is a potent inhibitor of PARP-1 activity in vitro and in vivo in rats. Acute (80 min) and prolonged (24h) focal cerebral ischaemia was induced in rats by obstruction of the median cerebral artery, with or without reperfusion, with or without administration of 5-AIQ. The oxidative activity of neutrophils was measured by chemiluminescence. Administration of 5-AIQ.HCl (3.0 mg kg-1 b.w. - i.v.) caused a significant decrease in the oxidative activity of neutrophils in the group which had experienced chronic ischaemia for 24h but had no significant effect in the group which had received 80 min ischaemia, when compared to the control group. Increase of the oxidative activity of neutrophils was confirmed in rats with prolonged cerebral ischaemia, followed by reperfusion. 5-AIQ probably may decrease this activity through inhibition of PARP-1 in focus of local ischaemia as well as hence lowering the expression of inflammatory mediators by activated neutrophils.
4
Content available remote

Administration of low doses of tumor necrosis factor-alpha protects rat liver from ischaemic damage and reperfusion injury

64%
Helewski K. J., Kowalczyk-Ziomek G. I., Czecior E., Swietochowska E., Wielkoszynski T., Czuba Z. P., Szliszka E., Krol W.
Journal of Physiology and Pharmacology
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2010
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tom 61
|
nr 3
273-278
Liver ischaemia and reperfusion (IR) injury is a significant clinical problem. The aim of our study was to investigate the protective effect of tumor necrosis factor-alpha (TNF-) on rat liver ischaemia-reperfusion injury. A TNF- dose of 3 µg/kg body weight was injected into rats that had undergone partial (70%) ischaemia and reperfusion. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), total blood antioxidant level (using the FRAP test), and the concentrations of TNF-, myeloperoxidase (MPO) and malondialdehyde (MDA) in liver homogenates after 1, 6, and 72 hours of reperfusion were measured. It was demonstrated that, rats subjected to IR, the administration of small doses of TNF- significantly reduced ALT and AST activities after 60- minute liver ischaemia and 1 or 6 hour of reperfusion. The strongest reductions in ALT and AST activities were seen after 1 hour of reperfusion (30% and 35%, respectively). Exogenous TNF- reduced the release of this cytokine in all observed periods, with the greatest reduction observed after 1 hour of reperfusion. Decreases in MPO concentration (by 40-45% in all periods of observation), as a marker of hepatic neutrophil infiltration, and in MDA concentration, the end-product of lipid peroxidation (by 55-60% at all time points), accompanied the reduction of TNF- release. The administration of TNF- to the rats after IR did not alter total plasma antioxidant potential, as assayed by the FRAP test, after 1 hour of reperfusion; however, at the later times a marked increase (~ 40-50%) occurred. We demonstrated that intraperitoneal injections of small doses of TNF- protect rat livers from IR injury. The mechanism of this protection is related to reductions in the release of TNF- during IR after injection of this cytokine, resulting in reductions in oxidative stress and inflammation during the later phase of reperfusion.
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