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1

Nicotinamide and 1-methylnicotinamide reduce homocysteine neurotoxicity in primary cultures of rat cerebellar granule cells

100%
Slomka M., Zieminska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2008
|
tom 68
|
nr 1
Nicotinamide is an important cofactor in many metabolic pathways and a known neuroprotective substance, while its methylated product, 1-methylnicotinamide, is a suspected neurotoxin. Homocysteine is a risk factor in Alzheimer’s disease and neurodegeneration, causing inhibition of methylation processes and inducing excitotoxicity. In this study, using primary cultures of rat cerebellar granule cells and propidium iodide staining, we investigated the neurotoxicity of nicotinamide and 1-methylnicotinamide, and their neuroprotective potential in acute and sub-acute homocysteine neurotoxicity. Our results demonstrated that nicotinamide and 1-methylnicotinamide applied for 24 h to cultures at concentrations of up to 25 mM had no effect on neuronal viability. Moreover, nicotinamide at concentrations of 5–20 mM and 1-methylnicotinamide at 1–10 mM applied to cells 24 h before, and for 24 h after an acute 30 min application of 25 mM D,L homocysteine, reduced neuronal damage. 1-Methylnicotinamide at concentrations of 250 and 500 µM showed neuroprotective activity during a sub-acute 24-h exposure to 2.5 mM D,L-homocysteine, while 5 and 25 mM nicotinamide also evoked neuroprotection. These findings do not support suggestions that 1-methylnicotinamide may act as an endogenous neurotoxic agent; rather, they indicate the neuroprotective ability of nicotinamide and 1-methylnicotinamide in homocysteine neurotoxicity. The exact mechanisms of this neuroprotection are unclear and require further investigation.
2

Inhibition of mGluR1 and mGluR5 impairs memory consolidation and reconsolidation by disregulation of local protein synthesis

100%
Slomka M., Lenart J., Salinska E.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
It is known that mGluRs group I (mGluR1 and mGluR5) are involved in memory consolidation and reconsolidation probably by local protein synthesis regulation. One of the consequences of group I mGluRs activation is the synthesis of new proteins that play important role in memory consolidation and reconsolidation – NCAM and CaMKII, and also FMRP, that plays an important role in the mRNA transport and regulation of mRNA translation in the nerve endings by a negative-feedback mechanism. The aim of this study was to investigate the effect of mGluR1 and mGluR5 inhibition on synthesis of NCAM, CaMKII and the regulatory protein FMRP. In our experiments the passive avoidance task in one-day chicks was used and mGluRs 1/5 were inhibited by intracerebral injection of specific inhibitors, LY367385 and MPEP respectively. The expression of chosen proteins was determined in nerve endings isolated from chick brain. Our results show, that inhibition of each receptor around the time of training resulted in decrease of NCAM and CaMKII synthesis, as well as in synthesis of FMRP. However, the inhibition of mGluR1/5 around the time of reminder resulted in increase in NCAM and CaMKII synthesis, although synthesis of FMRP was significantly decreased. These results suggest that both receptors are involved in memory formation by regulation of termination of protein synthesis through control of FMRP synthesis.
3

Hospitalization frequency caused by inflammatory bowel disease in rural and urban inhabitants

100%
Cichoz-Lach H., Celinski K., Slomka M.
Polish Journal of Environmental Studies
|
2010
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tom 19
|
nr 5
The purpose of our study was to analyze hospitalizations for inflammatory bowel disease noted in the Department of Gastroenterology, Medical University of Lublin. Cases of patients hospitalized in the Department of Gastroenterology, Medical University of Lublin in 1997-2007 were retrospectively analyzed. The material studied included patients’ case histories and medical records that were used to select such patients whose hospitalizations were caused by ulcerative colitis and Crohn’s disease. Analysis distinguished two groups: rural and urban inhabitants. In 1997-2007 there were 1,825 hospitalizations for the inflammatory bowel disease noted at our clinic, which was 12.15% of all hospitalizations: 8.54% patients with ulcerative colitis and 3.61% with Crohn’s disease. Among them, 30.47% were rural inhabitants while 69.53% of patients lived in towns. The observation data demonstrated that there has been a significant increase of patients with inflammatory bowel disease in the last decade, and the patients originating in urban areas were more frequent than those from rural regions. This may be related to environmental differences between these two population groups.
4

Neuroprotective potential of imethylnicotinamide in homocysteine-induced neurotoxicity in vitro

100%
Slomka M., Zieminska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
5

TRP channels participare in memory formation in passive avoidance task in one day old chicks

100%
Salinska E., Stafiej A., Slomka M.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Influx of calcium ions (Ca2+) into neurons after stimulation of glutamate receptors is a crucial step in intracellular cascade of memory formation. Recent findings showed the existence of additional mechanism involved in intracellular Ca2+ increase and triggered not by external signal but by internal signals like increase of Ca2+ within the cell and activation of G protein coupled receptors. We are talking here about transient receptor potential (TRP) channels. The aim of our study was to investigate the participation of TRP channels, especially TRPC and TRPV in intracellular mechanisms engaged in memory consolidation. METHODS: The model of passive avoidance task on one day old chicks was used. Chicks were injected with TRP channels antagonist SKF96365 and three different concentrations of 2-APB, the inhibitor of IP3 receptors, which in small concentrations inhibits also TRP channels. The injections were made at different times before and after training, to find the most effective time of interference. RESULTS: We found that injection of all antagonists immediately after training resulted in task amnesia when tested 24 h later. The amnesic effect of injection of SKF96365 or 2-APB immediately after training was tested at different times. It appeared that SKF96365 injection resulted in constant amnesia that manifested 1.5 h after training, whereas amnesia after injection of 2-APB was observed as early as 30 min after training. The effect of application of TRP channels antagonist SKF96365 on memorizing of the task in comparison with the effects of mGluR1 and mGlR5 antagonists showed similarities when memory was tested 2 h and 24 h training. CONCLUSIONS: Our results show that inhibition of TRP channels results in disturbance in memory formation and that inhibition of both TRP channels and IP3 receptors using small concentrations of 2-APB has a strong impact on this process.
6

COX-2/PGI2 pathway is involved in neuroprotection induced by N1-methylnicotinamide in hypoxia/ischemia of newborn rats

100%
Slomka M., Ziembowicz A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
1-Methylnicotinamide (MNA) is a key metabolite of nicotinamide, which is an important cofactor in many metabolic pathways with intrinsic cytoprotective properties. Recent studies demonstrated that MNA induces in the periphery the anti-inflammatory and vasoprotective effects mediated by the COX-2/ PGI2 signaling pathway. The role of this pathway in the protection against ischemic injury has been emphasized by the increased risk of myocardial infarction, stroke or susceptibility to excitotoxic insults caused by COX-2 inhibitors. This suggests that administration of MNA resulting in activation of COX-2/PGI2 might provide neuroprotection in brain ischemia. The aim of this study was to evaluate neuroprotective abilities of MNA in the model of brain hypoxia/ischemia (HI) in 7-day old rat pups, and to assess its effects on COX-2 activity and eicosanoid levels in the ischemic brain. The results demonstrated that i.p. administration of 62.5 mg/kg MNA 30 min after HI induced a significant neuroprotection and a marked increase in COX-2 activity 6 and 24 h after the insult. This effect was not accompanied by changes in the COX-2 protein level, as measured with Western blotting. The analysis of the level of eicosanoids: 6-keto-PGF1alpha-a which is a stabile metabolite of PGI2, PGE2, and TXB2 in brain of rats treated with MNA after HI demonstrated in the ipsilateral cortex a significant increase in 6-keto-PGF1alpha 30 min after the treatment, while PGE2 and TXB2 levels did not change. Pretreatment with rofecoxib (COX-2 inhibitor) or indomethacin (unselective COX inhibitor) decreased the level of 6-keto-PGF1alpha in the ipsilateral cortex to values observed in the untreated ischemic brain. To test the hypothesis that neuroprotection evoked by MNA in HI model depends on activation of prostacylin receptors, the selective antagonist of these receptors RO 324479 was applied. However, pretreatment of rat pups subjected to HI with RO 324479 (10 mg/ kg i.p.) did not influence significantly the neuroprotective effect of MNA. Further studies are needed to assess the role of COX-2/PGI2 in the MNA-evoked neuroprotection.
7

NMDA receptor antagonists MK-801 and memantine induce tolerance to oxygen and glucose deprivation in primary cultures of rat cerebellar granule cells

100%
Slomka M., Kuszczyk M., Lazarewicz J. W., Makarewicz D.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 4
Preconditioning is an experimental strategy for reducing ischemic brain damage. There are reports that brief exposure of neurons to NMDA-receptor antagonists may be an adequate preconditioning stressor. We studied effects of preconditioning of the cerebellar granule cells (CGC) in primary culture by 30-minute exposure to NMDA receptor antagonists 0.5 ^M MK-801 or 5 ^M memantine. CGC were challenged with oxygen and glucose deprivation (OGD) or excitotoxic glutamate and cell viability was tested 24 h later using calcein/ethidium homodimer-1 staining. We studied glutamate-induced increases in 45Ca uptake and in the intracellular Ca2+ level assessed with the fluorescent probe fluo-3. The number of living cells in OGD-treated cultures decreased by 42%. Preconditioning with MK-801 or memantine 24 h earlier reduced cell death to 8% and 30% and 48 h earlier to 27% and 33%, respectively. Pretreatment with MK-801 followed by the standard MK-801 wash out was slightly cytoprotective in a glutamate excitotoxicity test performed immediately; the protection increased significantly 24 h after preconditioning. In both cases the extensive wash out of MK-801 after preconditioning resulted in loss of cytoprotection. The increase in the intracellular Ca2+ level evoked by glutamate was decreased 24 h after preconditioning and even halved in the neuronal cultures 48 h after preconditioning with MK-801 and memantine. Glutamate-induced 45Ca uptake in these cells was decreased by 18%, irrespective of the time laps after preconditioning. These results demonstrate that preconditioning of CGC with NMDA receptor antagonists induces prolonged tolerance to OGD, which is accompanied by the reduction of glutamate-evoked calcium fluxes. The causal relationship between these effects may be suggested.
8

Analysis of putative toxic interaction of L-methylnicotinamide with dopaminergic neurons

100%
Slomka M., Ziembowicz A., Lazarewicz J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
It has been proposed that in the Parkinson’s disease exo- or endogenous N-methyl-compounds like 1-methylnicotinamide (MNA) could be accumulated by dopaminergic neurons and induces neurotoxic effects, as happens with MPP+. The aim of this study was to test this hypothesis by comparing direct effects of MPP+ or MNA application into the striatum of 7 day old rat pups and to the substantia nigra (SN) of the adult rats. Microinjections of tested substances in doses: MPP+ (20 and 100 μg) and MNA (20, 40, 80 μg), were made unilaterally. Effects of MNA and MPP+ on pups’ striatum were evaluated by TTC staining and the lesion volume was calculated using the ImageJ program. In the SN of adult rats alterations in the level of tyrosine hydroxylase (TH) immunostaining were examined at the 5th day after MPP+ or MNA injection, utilizing antibody specifi c to TH. Moreover the coronal sections (20 μm thick) of the SN were examined to evaluate MNA- or MPP+-induced glial activation with the glia-specifi c lectin. Using these methods we did not observe any toxic effect of MNA. MPP+ induced statistically signifi cant damages in the striatum of rat pups, whereas there was no lesion after MNA injection. Also in the SN of adult rats MPP+ caused 50% loss of TH-positive neurons and doubled the number of activated glial cells, while MNA injection had no visible effect. Summing up, present data did not demonstrate any toxic effects of MNA on dopaminergic neurons in the rat brain in vivo.
9
Content available remote

Pathophysiology of portal hypertension

100%
Cichoz-Lach H., Celinski K., Slomka M., Kasztelan-Szczerbinska B.
Journal of Physiology and Pharmacology. Supplement
|
2008
|
tom 59
|
nr 2
In last years significant progress in recognizing mechanisms of portal hypertension pathophysiology was done. However, some unclear topics in this disease still exist. Portal hypertension is primarily caused by the increase in resistance to portal outflow and secondly by an increase in splanchnic blood flow. Portal hypertension is associated with changes in the intrahepatic, systemic, and portosystemic collateral circulation. Alterations in vasoreactivity (vasodilation and vasoconstriction) play a central role in the pathophysiology of portal hypertension by contributing to increased intrahepatic resistance, hyperdynamic circulation, and expansion of the collateral circulation. Among vasoactive substances which are activated in portal hypertension nitric oxide (NO) is considered as the most important vasodilator. Endothelin-1 and cyclooxygenase-derived prostaglandins are the main vasoconstrictor factors. The imbalance between the hyperresponsiveness and overproduction of vasoconstrictors and the hyporesponsiveness and impaired production of vasodilators are the mechanisms responsible of the increased vascular tone in the sinusoidal area of the liver. New concepts in the pathophysiology of portal hypertension find the significant role of hepatic stellate cells activated by endothelial factors which cause vascular remodeling as an adaptive response of the portal vessels wall. The most frequent causes of portal hypertension include portal vein thrombosis, storage diseases of the liver, hepatic cirrhosis (independent of etiology), hepatic veins thrombosis and schistosomiasis. Understanding the pathophysiology of portal hypertension could be of great utility in preventing and curing the complications of portal hypertension, such as esophageal varices, hepatic encephalopathy, ascites.
10
Content available remote

The effects of L-tryptophan and melatonin on selected biochemical parameters in patients with steatohepatitis

88%
Cichoz-Lach H., Celinski K., Konturek P. C., Konturek S. J., Slomka M.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 5
11

Okreslanie opornosci na metycyline klinicznych szczepow Staphylococcus aureus w rutynowej diagnostyce mikrobiologicznej

88%
Slomka M., Szymanowska A., Rokosz A., Sawicka-Grzelak A., Luczak M.
Medycyna Doświadczalna i Mikrobiologia
|
2004
|
tom 56
|
nr 2
127-131
Przebadano wrażliwość na metycylinę 120 szczepów S. aureus wyhodowanych w laboratorium diagnostycznym Katedry i Zakładu Mikrobiologii Lekarskiej Akademii Medycznej w Warszawie z zastosowaniem dwóch metod: krążkowo-dyfuzyjnej i komercyjnej ATB STAPH S (wersja 2000). W przypadku 116 szczepów, co stanowiło ogółem 97% badanych szczepów, stwierdzono zgodne wyniki oznaczeń w obu metodach.
12

Blood serum ascorbic acid evaluated in patients suffering from liver and pancreas diseases and in the liver, heart, kidneys and lungs of rats intoxicated with CCl4 and galactosamine

76%
Madro A., Czechowska G., Szymonik-Lesiuk S., Celinski K., Slomka M., Stryjecka-Zimmer M.
Medycyna Weterynaryjna
|
2008
|
tom 64
|
nr 06
The aim of the study was to evaluate blood serum ascorbic acid levels in patients with hepatic cirrhosis, acute and chronic pancreatitis and in the liver, heart, kidneys and lungs of rats intoxicated with CCl₄ and galactosamine. The results revealed statistically significant increases in the blood plasma ascorbic acid levels in patients with acute and chronic pancreatitis and hepatic cirrhosis. In the group of patients with chronic pancreatitis, however, the blood plasma ascorbic acid levels were not different from the controls. In the group of control rats the highest ascorbic acid levels were observed in the liver and the lowest in the heart. In the intoxicated rats with CCl₄ and galactosamine the kidneys’ ascorbic acid contents increased significantly after administration of both toxins in single doses but decreased after 3-days of administration of CCl₄. In the liver, decreased ascorbic acid contents were observed after single doses of CCl4 and galactosamine, but after the 3-day administration its contents were increased. The content of ascorbic acid in the lung increased after each of the toxins used. In the heart, ascorbic acid contents decreased considerably after single and three-day CCl₄ and galactosamine administration as well.
13
Content available remote

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

76%
Celinski K., Dworzanski T., Korolczuk A., Piasecki R., Slomka M., Madro A., Fornal R.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
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.
14
Content available remote

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

76%
Celinski K., Dworzanski T., Fornal R., Korolczuk A., Madro A., Slomka M.
Journal of Physiology and Pharmacology
|
2012
|
tom 63
|
nr 6
15
Content available remote

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

76%
Celinski K., Dworzanski T., Fornal R., Korolczuk A., Madro A., Brzozowski T., Slomka M.
Journal of Physiology and Pharmacology
|
2013
|
tom 64
|
nr 5
16

Neuroprotective potential of methylnicotinamide versus liicotinamide in vivo and in vitro

76%
Slomka M., Makarewicz D., Zieminska E., Duszczyk M., Stafiej A., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
17
Content available remote

Effects of melatonin and tryptophan on healing of gastric and duodenal ulcers with Helicobacter pylori infection in humans

76%
Celinski K., Konturek P. C., Konturek S. J., Slomka M., Cichoz-Lach H., Brzozowski T., Bielanski W.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 5
18
Content available remote

Matrix metalloproteinases activity during the evolution of hypoxic-ischemic brain damage in the immature rat. The effect of 1-methylnicotinamide (MNA)

76%
Dragun P., Makarewicz D., Wojcik L., Ziemka-Nalecz M., Slomka M., Zalewska T.
Journal of Physiology and Pharmacology
|
2008
|
tom 59
|
nr 3
441-455
Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that degrade the extracellular matrix and carry out key functions during brain development. Apart from a physiological role, excessive activation of MMPs in brain tissue has been postulated to represent a pathway for cell death arising from ischemia. To evaluate the possible involvement of MMPs in the perinatal brain asphyxia, we exposed 7-day-old rats to hypoxia-ischemia (HI). Unilateral HI was administered by ligation of the common carotid artery followed by hypoxia (7.4% O2/92.6% N2) for 65 minutes. This insult is known to produce brain damage confined to the cerebral hemisphere ipsilateral to the arterial occlusion in > 90% of animals. HI resulted in a significant elevation of MMP-2 and MMP-9 activity in the ipsilateral forebrain. The maximum activation was found at 48 hours and 7-14 days after the insult. These results suggest that early and late induction of MMPs may play a role in neuronal death as well as in repair processes. The treatment of animals subjected to HI with 1-methylnicotinamide (MNA), the anti-inflammatory agent, led to the inhibition of MMP-9 in an acute phase of ischemic damage and to the activation of MMP-2 in the later stages after injury. The timing of MMPs modulation by MNA may indicate its possible therapeutic implications.
19

Changes in the levels of lipid peroxidation, thiol groups and ascorbic acid in rat tisues after carbon tetrachloride intoxication

76%
Szymonik-Lesiuk S., Stryjecka-Zimmer M., Czechowska G., Slomka M., Madro A., Wielosz M.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
20
Content available remote

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

76%
Celinski K., Konturek P. C., Slomka M., Cichoz-Lach H., Brzozowski T., Konturek S. J., Korolczuk A.
Journal of Physiology and Pharmacology
|
2014
|
tom 65
|
nr 1
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