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1

Wpływ stopnia zagęszczenia soków truskawkowych na zmiany wybranych wyróżników jakościowych podczas przechowywania

100%
Kalisz S., Mitek M., Cendrowski A., Leskiewicz M.
Zeszyty Problemowe Postępów Nauk Rolniczych
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2011
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tom 569
Określono wpływ stopnia zagęszczenia soków truskawkowych na wybrane wyróżniki jakościowe. Zakres przeprowadzonych badań obejmował wyprodukowa­nie zagęszczonych soków truskawkowych (45, 55, 65°Bx) i ocenę wpływu stopnia zagęszczenia na zawartość cukrów, polifenoli ogółem, w tym zawartości antocyjanów i stopnia ich degradacji, zawartość katechin, pojemność przeciwutleniającą, a także parametry barwy. Analizy wykonywano bezpośrednio po wytworzeniu za­gęszczonych soków oraz po 1, 2, 3, 4 miesiącach ich przechowywania w temperaturze -18°C. W trakcie 4 miesięcznego przechowywania nastąpiło pojaśnicnie barwy od 5% (przy zagęszczeniu do 45°Bx) do 9% (65°Bx) oraz obniżenie aktywności przeciwutleniającej od 13% (45°Bx) do 27% (65°Bx). Wykazano również zmniej­szenie zawartości antocyjanów i związków polifenolowych średnio o 14%, a sto­pień zagęszczenia nie wpłynął zasadniczo na dynamikę tych zmian. Zwiększenie stopnia zagęszczenia powodowało wzrost degradacji barwników antocyjanowych. Stwierdzono również istotny wpływ czasu przechowywania zagęszczonych soków truskawkowych na zmianę parametrów barwy badanych koncentratów.Określono wpływ stopnia zagęszczenia soków truskawkowych na wybrane wyróżniki jakościowe. Zakres przeprowadzonych badań obejmował wyprodukowa­nie zagęszczonych soków truskawkowych (45, 55, 65°Bx) i ocenę wpływu stopnia zagęszczenia na zawartość cukrów, polifenoli ogółem, w tym zawartości antocyjanów i stopnia ich degradacji, zawartość katechin, pojemność przeciwutleniającą, a także parametry barwy. Analizy wykonywano bezpośrednio po wytworzeniu za­gęszczonych soków oraz po 1, 2, 3, 4 miesiącach ich przechowywania w temperaturze -18°C. W trakcie 4 miesięcznego przechowywania nastąpiło pojaśnicnie barwy od 5% (przy zagęszczeniu do 45°Bx) do 9% (65°Bx) oraz obniżenie aktywności przeciwutleniającej od 13% (45°Bx) do 27% (65°Bx). Wykazano również zmniej­szenie zawartości antocyjanów i związków polifenolowych średnio o 14%, a sto­pień zagęszczenia nie wpłynął zasadniczo na dynamikę tych zmian. Zwiększenie stopnia zagęszczenia powodowało wzrost degradacji barwników antocyjanowych. Stwierdzono również istotny wpływ czasu przechowywania zagęszczonych soków truskawkowych na zmianę parametrów barwy badanych koncentratów.
2
Content available remote

Excitatory neurosteroids attenuate apoptotic and excitotoxic cell death in primary cortical neurons

100%
Leskiewicz M., Jantas D., Budziszewska B., Lason W.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 3
457-475
Some neurosteroids show neuroprotective action in in vitro and in vivo studies, but their interaction with apoptotic/necrotic processes has been only partially unraveled. The aim of the present study was to examine the effect of dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), pregnenolone (PGL) and allopregnanolone (Allo) on staurosporine-, glutamate-, and NMDA-induced damage in primary cortical neuronal culture. DHEA, DHEAS and PGL (0.1 and 1 µM) inhibited the staurosporine-evoked LDH release and decreased the number of apoptotic cells as shown by Hoechst`s staining, whereas Allo was without effect. The neurosteroids affected neither the staurosporine-evoked changes in caspase-3 activity nor the decrease in mitochondrial membrane potential. It was also shown that protective effects of DHEA, DHEAS and PGL against staurosporine-induced LDH release were attenuated by extracellular signal-regulated kinase (ERK) - mitogen-activated protein kinase (MAPK) inhibitor – PD 98059 (5 µM) but not by phosphatidylinositol-3-kinase (PI3-K) inhibitors such as LY 294002 (1 µM) or wortmannin (10 nM). The involvement of ERK2-MAPK in protective effects of neurosteroids was confirmed by Western blot study. Further study demonstrated that glutamate-induced cell damage was attenuated by DHEA, DHEAS, and PGL, but not by Allo. None of the steroids influenced NMDA-induced LDH release. The results of the present in vitro studies suggest that excitatory neurosteroids DHEA, DHEAS and PGL at physiological concentrations participate in the inhibition of cortical neuronal degeneration elicited by staurosporine and glutamate, whereas the most potent positive modulator of GABAA receptor - Allo - has no effect. Moreover, neurosteroids appear to attenuate the staurosporine-induced cell damage in a caspase-3 independent way and their neuroprotective mechanism of action involves the increase in ERK-MAPK phosphorylation.
3

Effects of neurosteroids on apoptotic processes in neuronal cells in vitro

100%
Lason W., Leskiewicz M., Budziszewska B., Regulska M.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
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nr 4
4
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Effect of allopregnanolone on D-[3H]-aspartate release and [3H]-glutamate uptake in the hippocampus of kainate-treated mice

100%
Leskiewicz M., Budziszewska B., Jaworska-Feil L., Lason W.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 2
In order to determine whether the status epilepticus leads to alterations in the neurosteroid effect on excitatory amino acid transmission, we studied the influence of allopregnanolone on aspartate release and glutamate uptake in mouse hippocampus at various times after kainate administration. No significant differences in the K+-stimulated D-[3H]-aspartate release from the hippocampi of saline- and kainate-treated mice were observed; however, that parameter tended to fall in tissues collected 1h after kainate administration. Allopregnanolone significantly attenuated the K+-stimulated D-[3H]-aspartate release from the hippocampi of control animals, as well at 24 h and 7 days after kainate injection; in contrast it did not affect amino acid release from the hippocampi collected 1 h after kainate administration. Kainate administration had no effect on [3H]-glutamate uptake after 1 and 24 h, but elevated that parameter on day 7. Allopregnanolone (10 and 100 µM) did not affect [3H]-glutamate uptake in control and kainate-treated mice. In conclusion, the present study indicates a loss of the inhibitory effect of allopregnanolone on the potasium-stimulated D-[3H]-aspartate release from mouse hippocampus during the kainate-induced status epilepticus; moreover, it excludes involvement of this neurosteroid in the regulation of hippocampal [3H]-glutamate uptake in both control and kainate-treated mice.
5

An involvement of phoshatidylinositol 3-kinase in anti-apoptotic action of l,25-dihydroxyvitamin D3 and its low-calcemic analogues in SH-SY5Y celi line

88%
Regulska M., Leskiewicz M., Budzszewska B., Kutner A., Lason W.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
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nr 4
6

Lymphangioinvasion in routine H and E staining is strongly associated with poor clinical outcome in lymph node-negative cutaneous melanoma patients

88%
Donizy P., Kaczorowski M., Halon A., Leskiewicz M., Matkowski R.
Folia Histochemica et Cytobiologica
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2016
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tom 54
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nr 3
7

The effect of TRH and its analogs on hydrogene peroxide-induced toxicity in differentiated human neuroblastoma SH-SY5Y cells

76%
Jaworska-Reil L., Budziszewska B., Leskiewicz M., Regulska M., Lipkowski A. W., Lason W.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
|
nr 4
8

Effects of neurosteroids on neuronal survival: Molecular basis and clinical perspectives

76%
Leskiewicz M., Budziszewska B., Basta-Kaim A., Zajac A., Kacinski M., Lason W.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
|
nr 4
Neurosteroids have long been known to act as important modulators of central nervous system functions. The concept of their mechanism of action, however, have essentially undergone an evolution. Previously, these compounds were postulated to regulate neuronal function mainly via allosteric regulation of some membrane-bound receptors, such as GABAA and NMDA receptors, in a non-genomic way. Recent studies have provided evidence for intracellular targets for neurosteroids, e.g., transcription factors (NFk-B, progesterone receptors), protein kinases (phosphatidylinositol 3-kinase, protein kinase C), or microtubule-associated proteins, i.e. factors essential in regulation of neuronal survival and apoptosis. This paper reviews in vitro and in vivo data on neurosteroid involvement in the regulation of neurodegenerative processes with emphasis on new intracellular and genomic mechanisms of their action. Potential utility of neurosteroids in the treatment of some neurodegenerative disorders has been also discussed.
9

Brain level of FKBP-51, a glucocorticoid receptor cochaperone, is decreased in a neurodevelopmental animal model of schzophrenia

76%
Basta-Kaim A., Budziszewska B., Kabera M., Leskiewicz M., Regulska M., Korzeniak B.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
Recent studies suggest that dysregulation of the HPA axis activity and disturbance in glucocorticoid receptor (GR) action are involved in the pathogenesis of schizophrenia. The hyperfunction of GR can result from alterations in GR phosphorylation status or numbers of its cochaperones. The most important GR cochaperone FKBP-51, is known to inhibit GR transcriptional activity. The aim of the present work was to investigate the concentration of the immunophilin FKBP-51 in the hippocampus and frontal cortex in a neurodevelopmental animal model of schizophrenia. This model is based on administration of lipopolysaccharide to pregnant rats (in the second and third week of pregnancy). Amount of FKBP-51 was measured by Western blot method. In order to verify the above model, exploration, effi cacy of sensorimotor gating and performance in the social interaction test were determined. Prenatal LPS treatment induced behavioral disturbances typical of schizophrenia, like sensorimotor gating defi cit, higher exploratory activity and changes in social interaction test in the adult offspring. Furthermore, the level of the immunophilin FKBP51 was lower in both female and male offspring. These results suggest that multiple administrations of LPS to pregnant rats evoke GR hyperfunction in adult offspring by decreasing the concentration of FKBP-51, a protein which is known to inhibit GR function. This study was partially supported by the grant N40101231/0174 from the MSHE, Warsaw, Poland.
10

Inhibitory effect of neurosteroids on gluicocorticoid receptor-mediated gene transcription:an involvement of protein kinases and interaction with psychotropie drugs

76%
Leskiewicz M., Basta-Kaim A., Budziszewska B., Tetich M., Otczyk M., Lason W.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
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nr 3
11

Immunomodulatory effect of antidepressant drugs in animal models of depression

64%
Kubera M., Basta-Kaim A., Budziszewska B., Jaworska-Feil E., Roman A., Leskiewicz M., Telich M., Korzeniak B., Lason W.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
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nr 3
12
Content available remote

The decrease in JNK- and p38-MAP kinase activity is accompanied by the enhancement of PP2A phosphatase level in the brain of prenatally stressed rats

64%
Budziszewska B., Szymanska M., Leskiewicz M., Basta-Kaim A., Jaworska-Feil L., Kubera M., Jantas D., Lason W.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 2
Our previous study suggests that in prenatal stress model of depression glucocorticoid receptor (GR) function in adult rats is enhanced. However, the long-term consequences of stress, a causal factor in depression, on intracellular elements involved into the regulation of GR function is poorly examined. Mitogen-activated protein kinases (MAPKs), activity of which is disturbed in depression, are important regulators of GR action, so they can mediate the effect of stress on GR function. Therefore, the aim of the present study was to investigate the levels of active phosphorylated forms of extracellular signal-regulated kinases (ERK), Jun N-terminal kinases (JNK) and the p38 kinase in the hippocampus and frontal cortex in rats subjected to prenatal stress. The concentration of MAP kinase phosphatase (MKP-1, MKP-2) and protein phosphatase-2A (PP2A), which dephosphorylate all forms of MAP kinases, were also determined. During verification of the applied model of depression, we found that prenatally stressed rats displayed high level of immobility in the Porsolt test and that the administration of imipramine, fluoxetine, mirtazapine and tianeptine for 21 days normalized this parameter. Western blot study revealed that rats subjected to prenatal stress had decreased levels of p-JNK1 and p-JNK2 in the hippocampus and p-p38 in the frontal cortex, but the concentrations of p-ERK1 and p-ERK2 were not changed. Chronic treatment with imipramine inhibited the stress-induced decrease in p-JNK1/2, while imipramine, fluoxetine and mirtazapine blocked changes in p-p38. PP2A phosphatase level was higher in the hippocampus and frontal cortex in prenatally stressed animals than in control rats. Chronic treatment with antidepressant drugs attenuated the stress-induced increase in the level of this phosphatase, but had no effect on its concentration in control animals. There was no significant difference in MKP-1 and in MKP-2 levels in both brain structures between control and prenatally stressed rats. The obtained results showed that prenatal stress decreased the levels of active form of JNK and p38, but enhanced PP2A phosphatase expression and most of these changes were reversed by antidepressant drugs. Since p-JNK and p-p38 are known to inhibit GR function their lowered levels may enhance glucocorticoid action. Furthermore, the increased PP2A concentration may intensify GR action not only by inhibition of JNK and p38 phosphorylation, but also by a direct influence on the process of GR translocation.
13

The effect of antidepressant drugs on delayed-type hypersensitivity reaction in beta2M-/-, TCRdelta-/- and CD1d mice

52%
Kabera M., Szczepanik M., Majewska M., Zemelka M., Leskiewicz M., Basta-Kaim A., Budziszewska B., Grygiel B., Regulska M., Korzeniak B., Jagla G., Nowak W., Lason W.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
Delayed-type hypersensitivity (DTH) is a T cell-mediated immune reaction that plays a major role in the pathogenesis of various infl ammatory disorders. One of the most characteristic DTH phenomena is contact hypersensitivity (CS) used to assess cellmediated immunity against tumor cells and microbes that survive within macrophages. Recently it was suggested that activation of immune system plays a role in etiology of depression and that antidepressive agents have negative immunoregulatory effects. Our present studies showed that chronic fl uoxetine and desipramine administration signifi cantly inhibited CS reaction to picryl chloride (PCL) in B10.PLwild type mice (by 58% and 48%, respectively, when compared to positive control) and their inhibitory effect was even stronger in TCRd knockout mice. On the other hand in b2m-/- and CD1d-/- mice the prolonged antidepressant administration did not affect CS reaction. PCL sensitization signifi cantly increased spleen weight and proliferative activity of splenocytes in B10PL, TCRd-/- and b2m-/- mice. Prolonged antidepressant treatment attenuated this effect but only in B10PL mice. Presented data might suggest that inhibitory effect of desipramine and fl uoxetine on CS reaction could be caused by their infl uence on CD8+ and NKT regulatory cells that attenuate T cell-mediated immune response.
14

Prophylactic use of desupramine in wistar rats with high stress-sensitivity increases resistance to experimental tumor metastasis

52%
Kubera M., Grygier B., Lewandowska D., Gruca P., Rogoz Z., Budziszewska B., Basta-Kaim A., Leskiewicz M., Korzeniak B., Jagla G., Nowak W., Lason W.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
The effect of antidepressant drugs on tumour progress in animals models of stress is very poorly recognized. Further more a role of susceptibility to stress in modulatory effect of antidepressant drug on tumour growth have not been studied. The aim of present study was to establish the effect of individual reactivity to stress and prophylactic two weeks desipramine administration on metastatic colonization of MADB 106 cells in lungs of Wistar rats. Rats were subjected by three weeks to chronic mild stress (CMS) model of depression and high-reactive and non-reactive rats were selected. Three months after CMS termination high-reactive and non-reactive animals were further subdivided: for two additional weeks the rats received daily injection of desipramine or saline. Tumor cells were injected two hours after last desipramine or saline administration. In stress-reactive, vehicle treated rats increase of number of lung metastasis in comparison to stress non-reactive, vehicle treated rats were observed. On the other hand chronic desipramine pretreatment signifi cantly increased survival rate and diminished number of lung metastasis in stress-sensitive animals although did not show such effect in stressresistant animals. Increase in rate of animal survival and decrease in lung metastasis can be connected with stimulatory effect of chronic desipramine pretreatment on NK cell activity. This study was supported by grant N40109732/2074 from Poland’s MS and HE.
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