Wyniki wyszukiwania - Biblioteka Nauki

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Wpływ długotrwałego podawania rutyny na pamięć przestrzenną i neuroprzekaźnictwo u szczurów

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Pyrzanowska J. , Blecharz-Klin K. , Piechal A. , Joniec-Maciejak I. , Widy-Tyszkiewicz E.

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2011

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tom 48

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

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Joniec-Maciejak I. , Wawer A. , Sznejder-Pachołek A. , Wojnar E. , Mirowska-Guzel D.

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nr Suppl.1

EN

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.

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

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Schwenkgrub J. , Zaremba M. , Joniec-Maciejak I. , Cudna A. , Mirowska-Guzel D. , Kurkowska-Jastrzebska I.

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tom 75

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nr Supl.

EN

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.

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

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Pyrzanowska J. , Piechal A. , Blecharz-Klin K. , Joniec-Maciejak I. , Graikou K. , Chinou J. , Widy-Tyszkiewicz E.

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nr 2

EN

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.

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

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Schwenkgrub J. , Joniec-Maciejak I. , Ciesielska A. , Sznejder A. , Wawer A. , Bankiewicz K. , Czlonkowska A. , Czlonkowski A.

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nr S

EN

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.

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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

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Sznejder A. , Joniec-Maciejak I. , Ciesielska A. , Schwenkgrub J. , Wawer A. , Bankiewicz K. , Czlonkowska A. , Czlonkowski A.

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nr S

EN

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.