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1

Transport drogowy zwierzat zywych

100%

Trzecinski E. , Lenkiewicz A.

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tom 02

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nr 12

12-15

2

Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes ?

80%

Rafalowska U. , Struzynska L. , Dabrowska-Bouta B. , Lenkiewicz A.

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nr 2

3

Astroglial reaction in the early asymptomatic phase of experimental autoimmune encephalomyelitis

70%

Grygorowicz T. , Sulkowski G. , Sulejczak D. , Lenkiewicz A. , Struzynska L.

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nr 3

EN

Under different pathological conditions activation of astrocytes of neuroprotective or neurotoxic nature is observed. There is a growing number of evidence that many pathological states of brain are characterized by very early active contribution of astrocytes to neurodegenerative axonal damage. Astroglia posses defense mechanisms against glutamate excitotoxicity (transporter systems) but may also contribute to the enhanced release of this potentially toxic amino acid trough exocytosis, P2X7 purinergic receptors, hemichannels or reversing of glutamate transporters. These cells are also a main source of ATP, active signaling molecule, which activates many purinergic receptors in brain, including P2X7R, which participates in development of infl ammation and neurodegeneration phenomena. The aim of this study was to investigate the expression of astroglia-specifi c proteins during the course of EAE using immunochemical and immunohistochemical analysis. We observed early activation of astroglia in the inductive phase of EAE (4 day p.i.) which was connected with overexpression of GFAP and S-100β. Expression of Cx43, protein that forms hemichannels was also enhanced so as the expression of P2X7R. Additionally, the level of GLT-1 glutamate transporter’s protein increase signifi cantly. The results suggest that in EAE pathology very early activation of astroglia takes place in the preclinical stage of the disease. The exact nature of this activation will be investigated.

4

Glutamate receptors antagonists attenuate neurological deficits and modulate neuroinflammation in Lewis rat subjected to experimental autoimmune encephalomyelitis

70%

Sulkowski G. , Dabrowska-Bouta B. , Chalimoniuk M. , Lenkiewicz A. , Struzynska L.

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tom 73

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nr 1

EN

Experimental autoimmune encephalomyelitis (EAE) is an animal model that mimics many aspects of multiple sclerosis (MS). Chronic or relapsing inflammation of the central nervous system results in the destruction of myelin sheath and cytokines play an important role in the pathogenesis of both MS and EAE. Myelin, oligodendrocytes and neurons are lost due to an inflammatory attack by leukocytes infiltrating the central nervous system (CNS) and releasing cytotoxic cytokines, anti CNS antibodies and large amounts of the excitatory neurotransmitter glutamate. Pharmacological studies have suggested that glutamate receptors mediate white matter injury in a variety of CNS diseases, including multiple sclerosis (MS). Memantine and amantadine are ionotropic glutamate receptors (iGluRs) antagonists. Memantine, a clinically applied drug with N-methyl-D-aspartate (NMDA) receptor antagonistic effects, dose-dependently ameliorates neurological deficits in Lewis rats subjected to experimental autoimmune encephalomyelitis (EAE). The aim of the present study was to investigate the effects of memantine and amantadine on the expression of proinflammatory cytokines such interleukin 1beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and various chemokines in the brain of EAE rats. Real-time Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western Blot were used to analyze the cytokine profile. We noticed increased expression of array of cytokines in experimental group when compared to the control. Dramatic increase of IL-1β, IL-6, TNF-α, and chemokines concentration corresponding to the intensity of neurological symptoms and loss of weight was observed in EAE rats. Administration of iGluR antagonists at an advanced stage of unremitting EAE resulted in amelioration of the disease. Cytokine analysis revealed that memantine significantly decreased the expression of interleukins: IL-6 (65%), IL-1β (60%) and TNF-α (45%) whereas treatment with amantadine reduced only the expression of IL-6 (60%) and TNF-α (15%) when compared to EAE animals. These results show that antagonists of iGlu receptors modulate the course of the disease by reducing the expression of proinflammatory cytokines thereby confirming the involvement of glutamate receptors into pathological mechanisms operating during EAE. This study was supported by grant nr NN401620038 from Polish Ministry of Science and Higher Education

5

Ultrastructural and biochemical changes in brain of rat chronically exposed to silver nanoparticles

61%

Widynska J. , Dabrowska-Bouta B. , Frontczak-Baniewicz M. , Lenkiewicz A. , Grygorowicz T. , Struzynska L.

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nr Suppl.1

EN

Silver nanoparticles (AgNPs) demonstrate strong antimicrobial activity resulting in their wide-spread use in different applications, including medical ones. Despite of the fact that human exposure to nanosilver is constantly increasing, there is no many research dedicated for investigating their potential neurotoxic effects. Most of the previous studies on mechanisms of nanosilver neurotoxicity have used in vitro models. The aim of the present study was to determine whether this small-sized commercially available AgNPs induce ultrastructural and biochemical changes in brain of male adult rats. Rats were exposed orally to 10 ± 4 nm nanosilver in size for 14 days. Using transmission electron microscopy (TEM), nanosized granules were detected in brains of exposed rats. Besides, ultrastructural changes in cortical and hippocampal neurons were found. TBARs level was measured to assessed lipid peroxidation in homogenates from exposed animals and immunochemical analysis was used to measure the level of selected tissue markers of oxidative stress in brain. Supported by grant nr NN401619938.