Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 23

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1

Peripheral antinociceptive effect of MU and kappa opioid receptor agonists in normotensive wistar (NR), wistar Kyoto (WKY) and spontaneousily hypertensive rats (SHR)

100%
Mierzejewski P., Widy-Tyszkiewicz E., Kohutnicka M., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
1992
|
tom 52
|
nr 3
2

Interleukin-6 secretion by glial cells in Parkinson's disease mouse model

100%
Kurkowska-Jastrzebska I., Kohutnicka M., Czlonkowski A., Czlonkowska A.
Acta Neurobiologiae Experimentalis
|
1995
|
tom 55
|
nr 5
3

The contribution of the hypertensive state to the experimental model of chronic pain

100%
Kohutnicka M., Widy-Tyszkiewicz E., Mierzejewski P., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
1992
|
tom 52
|
nr 3
4

Simvastatin did not protect dopaminergic neurons from damage caused by MPTP

88%
Kurkowska-Jastrzebska I., Joniec I., Balkowiec-Iskra E., Czlonkowski A., Czlonkowska A.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
5

Reaction of microglial cells and lymphocytes after 1-methyl-4-phenyl-I ,2,3,6-tetrahydropiridine intoxication in mice

88%
Kurkowska-Jastrzebska I., Kohutnicka M., Wronska A., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
1997
|
tom 57
|
nr 5
6

Different immune response of brain areas and the inolvement of inflammatory cytokines (IL-1, IL-6, TNFalfa) in spatial learning and memory deficits after MPTP injury in mice

88%
Zaremba M., Kurkowska-Jastrzebska I., Cudna A., Piechal A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Parkinson’s disease (PD) is a neurodegenerative disorders causing not only motor dysfunction, but also cognitive disturbance. The pattern of cognitive deficits in PD often includes: executive impairments, episodic memory deficits and visuospatial dysfunctions. It also became evident that inflammatory processes play an important role in the pathophysiology of PD. Neurodegeneration intense brain immune activation and “cytokine storm” which might induce hyper-excitability of neuronal circuits and might reduce neuronal plasticity and cause impairments in learning and memory abilities. The role of cytokines in regulation of inflammatory responses in different brain regions during PD is unclear. It still remains to be fully understood as to how cytokines participate in the molecular and cellular mechanisms of deficits in learning, memory and cognition in PD. Loss of dopaminergic neurons in acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models is associated with massive and prolonged glial response and increased production and release of inflammatory mediators. To assess the inflammatory response following MPTP intoxication, we measured the IL-6, IL-1β and TNFα gene expression by real-time quantitative RT-PCR following the Morris water maze behavioral test that was provided at 7 days, 3 and 6 months from the intoxication. Our results indicate that neuroinflammatory activity in MPTP model was not restricted to the nigrostriatal system but also involved hippocampal and cortical areas, regions there are essential for cognitive functions such as working and long - term memory, not only in mice. To evaluate spatial learning and memory abilities of mice the mean latency of reaching the platform, the swimming distance, the time spent in the goal quadrant and crossing parameters were estimated. We found that these parameters correlated with level of mRNA expression of cytokines in hippocampus and cortex.
7

MHC class II positive microglia and lymhocytic infiltration are present in the substantia nigra and striatum in mouse model of Parkinson's disease

88%
Kurkowska-Jastrzebska I., Wronska A., Kohutnicka M., Czlonkowski A., Czlonkowska A.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 1
8

Post intoxicative therapeutic immunization with myelin oligodendrocyte glycoproteine [MOG 35-55] suppresses spontaneous regeneration of dopaminergic neurons injured with 1-methyl-4 phenyl-1,2,3,6-tetrahydropiridine [MPTP]

88%
Balkowiec-Iskra E., Kurkowska-Jastrzebska I., Joniec I., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2003
|
tom 63
|
nr 2
9

Age and gender influence on astrocyte activation in model of Parkinson's disease (PD)

76%
Ciesielska A., Joniec L., Przybylkowski A., Kurkowska-Jastrzebska I., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
10

Relationship between NOS expression and dopamine concentration in murine model of Parkinson’s disease

76%
Joniec I., Ciesielska A., Przybylkowski A., Kurkowska-Jastrzebska I., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
11

17Beta-estradiol application after MPTP intoxication prevents the depletion of tyrosine hydroxylase in striatum of aged małe mice

76%
Ciesielska A., Joniec I., Przybylkowski A., Kurkowska-Jastrzebska I., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
12

Dopamine, serotonin and noradrenaline changes in the striatum of C57BL mice following myelin oligodendrocyte glycoprotein (MOG) 35-55 and complete Freund adjuvant (CFA) administration

76%
Balkowiec-Iskra E., Kurkowska-Jastrzebska I., Joniec I., Ciesielska A., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2007
|
tom 67
|
nr 4
Many data suggest involvement of inflammation in neurodegeneration. However, the exact mechanisms of this cooperation are poorly understood. We have previously shown that induction of inflammatory reaction, both before and after injury of the striatum, affects regeneration of dopaminergic neurons. In the present research we studied the role of inflammatory reaction in non-injured striatum. We used myelin oligodendrocyte glycoprotein (MOG) 35-55 in complete Freund’s adjuvant (CFA) to elicit experimental autoimmune encephalomyelitis (EAE) mice model. As determined by HPLC, striatal dopamine (DA) and serotonin levels in mice treated with either MOG 35-55 in CFA or CFA alone were significantly higher compared to vehicle-treated controls on 13th day after induction. The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Noradrenaline (NA) concentration did not differ between groups. Moreover, the striatal mRNA IL-1ß and TNF-? levels were elevated during induction phase of EAE in both groups, as determined by RT-PCR. Our data indicate regulatory connection between dopaminergic and immune systems.
13

Long time effect of high doses glucocorticosteroids on mRNA expression for IL-6 and IL-8 in multiple sclerosis patients treated during relapse

76%
Mirowska-Guzel D., Gromadzka G., Kurowska K., Wicha W., Czlonkowski A., Czlonkowska A.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
14

Influence of dopaminergic system injury on working memory abilities

76%
Zaremba M. M., Kurkowska-Jastrzebska I., Joniec I., Piechal A., Blecharz-Klin K., Balkowiec-Iskra E. Z., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2007
|
tom 67
|
nr 3
15

Sex-dependent differences in the iNOS protein expression in a murine model of Parkinson’s disease

76%
Joniec I., Ciesielska A., Przybylkowski A., Kurkowska-Jastrzebska I., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
16

Dynamics of expression of the mRNA for cytokines and inducible nitric synthase in a murine model of the Parkinson's disease

76%
Ciesielska A., Joniec I., Przybylkowski A., Gromadzka G., Kurkowska-Jastrzebska I., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2003
|
tom 63
|
nr 2
17

The influence of IL-10 on the inflammatory reaction changes in the mice after 1-methyl-4-phenyl-1,2,3,6-tertahydropyridine (MPTP) treatment

64%
Sznejder A., Joniec-Maciejak I., Ciesielska A., Schwenkgrub J., Wawer A., Bankiewicz K., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Parkinson’s disease (PD) is one of most frequent neurological disorder characterized by the loss of dopaminergic neurons in substantia nigra and striatum. The typical reaction of central neural system (CNS) on neurodegenerative processes is microglia activation and the inflammatory reaction. Microglia activation stimulates astrocytes response, playing important role in neuroimmune reaction. Microglia cells secrete two types of mediators of the inflammatory process: anti- and pro- inflammatory. In the first stage of Parkinson’s disease, pro-inflammatory cytokines have important meaning. We investigated the effect of an adenoassociated viral vector (AAV2) containing the complementary DNA (cDNA) for human interleukine 10 (hIL-10). The aim of the present study was to examine the evaluation of inflammatory reaction changes following increased concentration of hIL-10 in the murine model of PD induced by MPTP. Male C57BL mice 12 month-old were used in this study. AAV2 vector was bilateraly administered into striatum at 7, 21, 28 days prior to MPTP intoxication. We observed changes in the morphology of microglia cells, infiltration of lymphocytes T (population of CD3+, CD4+ and CD8+) and some differences in the level of one of the most important pro inflammatory cytokines – IL-1α. Our study showed that IL-10 is strongly involved in the inflammatory reaction in the murine model of Parkinson’s disease induced by MPTP. After MPTP intoxication we observed the increase of activated microglia cells, infiltration of lymphocytes T and higher level of IL-1α mRNA. AAV2-hIL-10-treated mice displayed a significant decrease in the activated microglia cells, elevated expression of IL-10 receptors observed on glia cells, strong infiltration of lymphocytes T (mainly CD4+ and CD3+, less CD8+) and minor expression of IL-1α mRNA. Further research must be conducted to provide more evidence of protective role of IL-10 in Parkinson disease.
18

Inhibitory effects of 17beta-estradiol on production of both molecular and cellular factors in neuroinflammatory reaction in model of Parkinson's disease

64%
Ciesielska A., Joniec L., Cudna A., Kurkowska-Jastrzebska L., Sznejder A., Zaremba N., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
The neuroprotective action of 17β-estradiol (E2) against 1-methyl4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown in both female and male mice, however the exact mechanisms of that phenomenon remain obscured. We studied the chronic effects of E2 (0.25 mg per pellet, 21-days release) administered 7 days prior (Experiment 1) to or 3 days after (Experiment 2) MPTP intoxication (40 mg/kg, i.p.) in C57BL aged male mice on neurodegenerative and infl ammatory processes in nigrostriatal pathway. We estimated striatal: tyrosine hydroxylase (TH), glial fi brillary acidic protein (GFAP) content (Western blotting); cytokines (TNFα, TGFβ1, IFNγ), trophic factor (GDNF) gene expression (RT-PCR); CD4+ and CD8+ cells infl ux (immunohistochemistry) at 1, 7, 21 (Exp. 1) and 7, 21 (Exp. 2) days post intoxication. E2 exerted a neuroprotective effect upon nigrostriatal system when administered prior but also when administered after intoxication (E2 attenuated the MPTP-induced loss of TH). E2 also decreased the GFAP content. MPTP caused a rapid increase of TGFβ1, TNFα and IFNγ. Pre-treatment with E2 decreased the early expression of TGFβ1 and IFNγ but failed to suppress the MPTP-induced increase of TNFα. E2 pre-treatment also induced an increase of the GDNF and CD4+ cells infl ux to the injured brain areas but decreased the CD8+ cells infi ltration. The neuroprotective effects of E2 indicated in MPTP model might mediate through a modulation of neuroinfl ammatory reaction in lesioned nigrostriatal system.
19

The effect of human interleukin-10 on the nitric oxide synthases expression in MPTP- based model of Parkinson's disease

64%
Schwenkgrub J., Joniec-Maciejak I., Ciesielska A., Sznejder A., Wawer A., Bankiewicz K., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Parkinson’s disease (PD) is a progressive degenerative disorder, which etiology and pathogenesis remains unknown. Post mortem analysis of PD brain and studies on neurotoxic animal models of PD have provided evidence to support the involvement of oxidative stress and neuroinflammatory processes in the pathogenesis of PD. The high level of nitric oxide (NO) is produced by iNOS during the neuroinflammatory process caused by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) treatment. Under pathological condition NO can easily react with superoxide to form peroxynitrite (ONOOˉ), which is a strong oxidant. In the present study was examined the influence of the increased concentration of IL-10 (an anti-inflammatory cytokine) on the NOS expression in mouse model of PD induced by MPTP. One year-old male C57Bl mice were used in this study. An adeno-associated viral vector expressing the gene for human interleukin-10 (hIL-10) was used to transduce striatal cells 4 weeks prior to MPTP intoxication. Mice were sacrificed at the different time intervals: 1, 7 and 21 days after MPTP injection. Immunohistochemical and western blot analyses provide evidence for the protective properties of AAV2-hIL-10 in the MPTP-induced model of PD. There were reduction in the dopaminergic neuron quantity in SNpc and tyrosine hydroxylase protein in the striatum after MPTP injections, whereas in the group additionally treated with AAV2-hIL10 neuroprotection was observed. Treatment with AAV2-hIL-10 suppressed the MPTP-induced increase in iNOS and 3-nitrotyrosine (3-NT) expression in the midbrain.
20

The molecular and behavioral changes in the long-term observations in mice model of Parkinson's disease

64%
Zaremba M., Joniec L., Piechal A., Pyrzanowska J., Kurkowska-Jastrzebska L., Ciesielska A., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
The pathogenesis of non-motor symptoms in Parkinson’s disease (PD) is complex and not fully understood, but is believed to be related to the widespread nature of dopaminergic dysfunction involving structures beyond the substantia nigra. Therefore we’ve also focused in our experiments on specifi c brain regions (e.g. hippocampus and prefrontal cortex) critically involved in spatial learning and memory processes. One year old C57/BL male mice received 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine (MPTP) 40 mg/kg, and control group received 0.9 % NaCl. To evaluate spatial learning and memory abilities, the Morris water maze (WM) behavioral test was provided after 6 months from the intoxication. The brain concentration of monoamines: dopamine (DA), noradrenaline (NA), 5 – hydroxytryptamine (5-HT) and amino acid: glutamate (Glu) were determined by using high – performance liquid chromatography (HPLC). Statistical signifi cances differences in monoamines levels between groups were noticed in hippocampus (NA, DA content) and prefrontal cortex (NA content). We didn’t notice signifi cant differences in the WM test parameters between MPTP and the control animals. Correlation between the results of the behavioral testing in the probe trial and the level of monoamines were calculated. Swim distance to reach the hidden platform was negatively correlated with NA level in the hippocampus (rp=−0.62, P<0.05). There is need for a further investigation to confi rm the role for NA in spatial memories.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.