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

Znaleziono wyników: 13

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 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 / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1

Olfactory sensivity deficit in the MPTP model of PD as a consequence of biochemical lateralization and noradrenergic depletion in the olfactory bulbs

100%
Boguszewski P. M., Zaremba M., Joniec-Maciejak I., Kurkowska-Jastrzebska I.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Parkinson disease (PD) is a more general disease than thought previously and involves prominent nonmotor manifestations (e.g. anosmia, hyposmia). Olfactory dysfunction can precede onset of motor symptoms by up to 10 years and they might provide biomarkers of the pathogenetic process. The initiating neurobiological bases for such disturbance are still elusive. However, recent findings suggest a degree of independence of olfactory dysfunction from nigrostriatal dopamine (DA). The aim of this study was to assess the extent of influence of biochemical imbalance in the left and right olfactory bulbs (OBs) on olfaction in old (1 or 1.5 year) mice caused by 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) intoxication. METHODS: The olfactory capability was evaluated using a battery set of olfaction tests: The Buried Food Test (BFT), Olfactory Discrimination Test (ODT), Olfactory Sensitivity Test (OST). Noradrenaline (NE) and DA metabolism was evaluated by High-performance liquid chromatography (HPLC) method. RESULTS: Intraperitoneal administration of MPTP caused significant reduction in NE and DA contents, observed mostly in the right OB at 7 and 180 days post intoxication. Interestingly, diminished noradrenergic projection and intensification of compensatory mechanism in the right OB exerted disturbing effect in some olfaction test (OST, BFT). Compared to controls, MPTP mice displayed insensitivity to low concentration odors in the OST and spend more time to find a buried food in the BFT. CONCLUSIONS: Results of the study strong indicate on lateralization in the OBs. Reasons for this phenomenon are unknown, although they may reflect lateralized differences in the function of the two sides of OBs. Diminished NE projection may play more important role in odor sensitivity than DA and may be related to dysfunction in odor recognition (hyposmia).The present findings seem to justify future studies about possible role of NE for therapeutic manipulation in PD.
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Cerebral administration of alpha-synuclein monomers modulates inflammatory reaction in nigro-striatal system

88%
Szneider-Pacholek A., Joniec-Maciejak I., Wawer A., Ciesielska A., Mirowska-Guzel D.
Journal of Pre-Clinical and Clinical Research
|
2019
|
tom 13
|
nr 1
3

Neuroprotective properties of cystamine in MPTP-induced murine model of Parkinson’s disease

88%
Wawer A., Joniec-Maciejak I., Sznejder-Pacholek A., Wojnar E., Mirowska-Guzel D.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: Parkinson’s disease (PD) is a common neurodegenerative movement disorder. It is characterized by a progressive degeneration of dopaminergic substantia nigra neurons projecting to the striatum, as well as, by an accumulation of intraneuronal Lewy bodies containing misfolded a‑synuclein. Neurodegeneration is coincident with a decrease in dopamine, the dopamine transporter, and the dopamine metabolites levels in PD brain. Current therapeutic approaches for the treatment of PD are only symptomatic and do not block neuronal loss. Recently, an enormous amount of work has been conducted to identify molecules that could be used as neuroprotective agents. One of them is cystamine – the inhibitor of transglutaminases activity. Transglutaminases are involved in the formation of a-synuclein aggregates, therefore blocking of its activity may prevent the progression of PD. AIM(S): The aim of the present study was to examine the effects of cystamine on neurodegenerative processes in the murine model of PD. METHOD(S): Male 1‑year‑old C57Bl/10 Tar mice were used in this study. Cystamine was injected intraperitoneally for 14 days, beginning 13 days prior to 1‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine (MPTP) intoxication. Changes in the mRNA level of inflammatory factors in striata were examined using Real‑Time PCR. Neurotransmitter levels in striata were evaluated by high‑performance liquid chromatography (HPLC). RESULTS: Our study demonstrated that chronic administration of cystamine before MPTP intoxication improved striatal levels of dopamine and its metabolites, as compared to MPTP‑treated groups. We also observed an inhibition of inflammatory reaction induced by MPTP (lower expression of microglia marker and proinflammatory interleukin). CONCLUSIONS: Cystamine exerts anti-inflammatory effects and preserves nigrostriatal function after MPTP intoxication in PD. However, further research must be conducted to provide more evidence of a protective role of cystamine in PD.
4

Cerebral administration of alpha synuclein modulates inflammatory reaction in the nigro striatal system: A comparison of males and females

88%
Sznejder-Pacholek A., Joniec-Maciejak I., Wawer A., Wojnar E., Mirowska-Guzel D.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: The risk of developing Parkinson’s disease (PD) is twice as high among men as among women. Estrogens appear to be a protective factor. The progression of PD is characterized by inflammation, especially the activation of the microglia. The data suggests that increased levels of α‑synuclein (ASN) can induce microglia activation. Activated microglial cells release pro‑ and anti‑inflammatory cytokines. AIM(S): The aim of this study was to investigate the role of increased ASN monomers concentration as a major pathogenic factor causing microglia response and changes in the expression of mRNA of inflammatory cytokines (i.e., interleukin 1α (IL‑ α), IL‑10, IL‑12 and tumor necrosis factor α (TNFα)) in the striatum (ST). We also examined the levels of ionized calcium binding adaptor molecule 1 (Iba‑1). We evaluated the differences between the genders after injection of ASN. METHOD(S): Male and female C57Bl/10 Tar 9-month- ‑old mice were used in this study. Human recombinant ASN was bilaterally administered into ST (single treatment – 4 μg/structure, 8 μg per brain) and mice were decapitated after 4‑or 12‑weeks post injection. Changes in the level of inflammatory factors in ST were evaluated using Real‑Time PCR. RESULTS: We observed increased levels of a microglia marker, Iba1 protein, in all experimental groups after 4 weeks of injection of ASN into the ST, with the highest differences in the FOVA group (female after ovariectomy). IL‑10 mRNA levels were significantly elevated in the FOVA group at 4 weeks after ASN administration intothe ST as compared to the ovariectomy control group. We noticed differences in levels of IL‑1α, IL‑12, and TNFα mRNA between the genders after injection of ASN. CONCLUSIONS: Our results support the hypothesis of pro‑inflammatory actions of ASN monomers. Injection of ASN into the ST induces microglia activation. Estrogens appear to be an important factor in the inflammatory reaction in the murine model of Parkinson’s disease after cerebral administration of ASN.
5

The effect of alpha-synuclein on initiation of inflammatory reaction in the murine brain

88%
Joniec-Maciejak I., Wawer A., Sznejder-Pachołek A., Wojnar E., Mirowska-Guzel D.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Parkinson’s disease (PD), one of the most common neurological disorder, is characterized by the loss of dopaminergic neurons in substantia nigra and striatum (ST). The typical reaction of central nervous system (CNS) on neurodegenerative processes is microglia activation and the inflammatory reaction. The data suggests that increased level of α‑synuclein (ASN), a small protein which is the major component of Lewy bodies, can induce microglia activation. Activated microglial cells release proinflammatory and potentially cytotoxic substances like cytokines. Till now, little is known about in vivo effects of exogenous ASN monomers on initiation of neuroinflammation and neurodegeneration. AIM(S): The aim of the present study was to examine the effect of increased ASN monomers concentration on microglia response and expression of pro‑ and anti‑inflammatory cytokines (interleukin 1α (IL‑1α), IL‑10, IL‑12) in the ST. METHOD(S): Male and female C57Bl/10 Tar mice 9 month-old were used in this study. Human recombinant ASN was bilaterally administered into ST (single treatment – 4 μg / structure, 8 μg per brain) and mice were decapitated after 4 or 12 weeks post injection. The changes in the level of inflammatory factors in ST were evaluated using Real-Time PCR and enzyme-linked immunosorbent assay (ELISA). RESULTS: We observed increased level of a microglia marker – ionized calcium-binding adapter molecule 1 (IBA1) protein after ASN injection into ST. We noticed also some differences in the level of one of the most important pro inflammatory cytokines – IL‑1α. CONCLUSIONS: Our study showed that monomers of ASN are strongly involved in the inflammatory reaction in the murine CNS. Further studies are required to reveal the detailed mechanism of the influence of ASN on neuroinflammation in course of Parkinson’s disease. FINANCIAL SUPPORT: This study was supported by Grant No 1M9/PM 2/16 (Medical University of Warsaw). Research subject was implemented with CePT infrastructure financed by the European Union – The Europan Regional Development Fund within the operational programme “Innovative economy for 2007–2013.
6

Wpływ długotrwałego podawania rutyny na pamięć przestrzenną i neuroprzekaźnictwo u szczurów

88%
Pyrzanowska J., Blecharz-Klin K., Piechal A., Joniec-Maciejak I., Widy-Tyszkiewicz E.
Annals of Warsaw University of Life Sciences - SGGW. Animal Science
|
2011
|
tom 48
7

The influence of alpha-synuclein on neurodegenerative processes in the murine brain

88%
Wojnar E., Wawer A., Joniec-Maciejak I., Sznejder-Pachołek A., Mirowska-Guzel D.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Parkinson’s disease (PD) is one of the most common neurodegenerative disorders. It is characterized by a progressive loss of dopaminergic neurons accompanied by a decreased concentration of dopamine (DA) and its metabolites in the striatum (ST). Experimental and clinical data indicate that α‑synuclein (ASN) plays an important role in many processes observed in the brains of patients with PD, such as disorder homeostasis of dopamine (DA) or initiate of oxidative stress. Changes in ASN levels due to its aggregation, overexpression or decreased expression may disrupt DA homeostasis and contribute to the neurodegeneration process observed in PD. AIM(S): The aim of the present study was to investigate the influence of cerebral injection of ASN on neurotransmitters level in ST. We also examine the expression of tyrosine hydroxylase gene (TH, the rate-limiting enzyme of catecholamine biosynthesis) and tissue transglutaminase 2 gene (TG2; an enzyme involved in aggregation of ASN). METHOD(S): Male and female C57Bl/10 Tar mice 9 month-old were used in this study. Human recombinant ASN was bilaterally administered into ST (4 μg/structure, 8 μg per brain) and mice were decapitated after 4 or 12 weeks post injection. Concentration of striatal neurotransmitters were measured by high performance liquid chromatography (HPLC). The gene expressions were examined by Real Time PCR. RESULTS: Intracerebral administration of ASN monomers led to changes in concentrations of striatal neurotransmitters but do not affect the expression of TH gene. The ASN administered intracerebrally into ST increases striatal expression of TG2 gene, which can lead to enhanced ASN aggregation. CONCLUSIONS: The biochemical changes observed after ASN administration may initiate further neurodegenerative processes and probably represent a very early stage in development of PD. Further research must be conducted to better understand the crucial role of ASN in the neurodegenerative process in PD. FINANCIAL SUPPORT: This study was supported by Grant No. 1M9/PM 2/16 (Medical University of Warsaw). Research subject was implemented with CePT infrastructure financed by the European Union – The Europan Regional Development Fund within the operational programme “Innovative economy for 2007–2013.
8

The influence of phosphodiesterase inhibitors on degradation and neuroinflammation in the mouse model of Parkinson's disease

76%
Schwenkgrub J., Zaremba M., Joniec-Maciejak I., Cudna A., Mirowska-Guzel D., Kurkowska-Jastrzebska I.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: A neuroprotective or disease modifying treatment of Parkinson’s disease (PD) still remains an unmet need. The non-clinical and clinical studies have indicated that cyclic nucleotide phosphodiesterase (PDE) inhibitors represent a novel class of drugs which may be useful in treating neuroinflammation disorders. The present study was designed to examine the efficacy of PDE inhibitors, ibudilast (IBD) and vinpocetine (VPC) in the mice model of PD induced by 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP). METHODS: 3 months-old male C57Bl/10Tar mice were treated with IBD (0, 20, 30, 40 or 50 mg/kg) BID for 9 days or VPC (0, 10, 20 or 30 mg/kg) once daily for 8 consecutive days (beginning 2 days or 1 day prior to MPTP (60 mg/kg) intoxication, respectively). Rotarod test was conducted on day 3 post MPTP injection. Mice were sacrificed 7 days after MPTP intoxication. IL-1β, IL-6, TNF-α and GDNF mRNA expression in the striatum was examined by the Real Time RT-PCR method. Western blot analysis was used to estimate tyrosine hydroxylase (TH) expression, micro- and astroglia activation markers (Iba1 and GFAP, respectively). Dopamine (DA) metabolism was evaluated by HPLC method. RESULTS: Chronic administration of PDE inhibitors attenuated astroglial reactivity and increased glial cell-derived neurotrophic factor (GDNF) gene expression in the striatum. IBD reduced TNF-α, IL-6 and IL-1β expressions, whereas VPC had no impact on elevated levels of TNF-α. Moreover,  mice receiving 40 mg/ kg IBD showed significant improvement in the locomotor activity compared to control. However, PDE inhibitors did not change DA metabolism and TH expression in the striatum. CONCLUSIONS: The findings provide evidence for the glia-derived protective properties of PDE inhibitors in the MPTP-induced model of PD. This response may be promising for the better outcome in the later stages of neurodegeneration. However, the further study is needed to confirm such possibility.
9
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Administration of Greek Royal Jelly produces fast response in neurotransmission of aged Wistar male rats

76%
Pyrzanowska J., Piechal A., Blecharz-Klin K., Joniec-Maciejak I., Graikou K., Chinou J., Widy-Tyszkiewicz E.
Journal of Pre-Clinical and Clinical Research
|
2015
|
tom 09
|
nr 2
Introduction. Royal Jelly (RJ) is a popular bee-derived product used widely in European and Asian traditional medicine. RJ has some pharmacological activities to support health and longevity as well as prevent ageing. Objectives. To evaluate whether a short-term 6-day Royal Jelly administration is able to induce behavioural and neurochemical effects in aged rats. Materials and method. RJ (previously chemically characterized by GC-FID and GC–MS) was given to 18-month-old male Wistar rats (100 and 500mg of powder/kg b.w./day) in subcutaneous injection for 6 days. Spatial memory was assessed in a water maze. Afterwards, the level of neurotransmitters, their metabolites and turnover in the selected brain regions were estimated by HPLC. Results. Short-term RJ administration did not change spatial memory in aged rats in the water maze, although it was sufficiently active to modify most of all the serotonergic and dopaminergic transmission in the prefrontal cortex and hippocampus. Conclusion. The obtained results indicate that Royal Jelly is able to affect very quickly the neurotransmission in the brain structures responsible for cognitive performance; however, short-term administration is not sufficient to exert behavioural consequences.
10
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Dihydroergotamine affects spatial behavior and neurotransmission in the central nervous system of Wistar rats

76%
Piechal A., Blecharz-Klin K., Joniec-Maciejak I., Pyrzanowska J., Krzysztoforska K., Mirowska-Guzel D., Widy-Tyszkiewicz E.
Annals of Agricultural and Environmental Medicine
|
2021
|
tom 28
|
nr 3
11

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.
12

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.
13

The influence of AAV-mediated gene transfer of human interleukin 10 on the neurodegenerative process in the murine model of parkinson's disease

64%
Wawer A., Joniec-Maciejak I., Schwenkgrub J., Sznejder A., Ciesielska A., Bankiewicz K., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Parkinson’s disease (PD) is one of the most common neurodegenerative disorders. It is characterized by a progressive loss of dopaminergic neurons, which occurs mainly in the substantia nigra (SN), resulting in the loss of nerve terminals, accompanied by a decreased concentration of dopamine (DA) and its metabolites in the striatum. Concurrently with neurodegeneration, a chronic inflammation occurs in the affected regions of the brain. Mechanisms and etiology of the neurodegeneration are still unknown. One potential strategy for therapy of PD is to reduce the neurodegeneration by inhibiting the inflammatory reaction. Nowadays, there are high hopes for the gene therapy based treatment. This involves using a noninfectious virus administered directly into the brain. In this study a transfer of AAV vector containing the complementary DNA for human interleukin 10 (IL-10) into the nigrostriatal pathway was used. IL-10 is one of the major antiinflammatory cytokines. The aim of the present study was to examine the expression of human IL-10, administered into striatum by viral vector AAV2-hIL-10 and investigate the influence of this cytokine on neurodegenerative process in the murine model of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). One year old male C57Bl mice were used in this study. The expression of human IL-10 was measured by enzyme-linked immunosorbent assay (ELISA). To evaluate the influence of the human IL-10 on neurodegeneration concentrations of striatal DA, 3,4-dihydroxyphenyl acetic acid and homovanillic acid were measured by high performance liquid chromatography (HPLC). The findings demonstrate human IL-10 secretion in the mouse brain after striatal infusion of AAV2-hIL-10. This study suggests that human IL-10 delivered by an AAV2 vector preserves nigrostriatal function after MPTP intoxication (lower decrease in DA concentration). IL-10 can play a vital role in inhibition of inflammatory reaction or surviving cells stimulation.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 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.