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1

A quantitative immunocytochemical study of blood-brain barrier to endogenous albumin in cerebral cortex and hippocampus of senescence-accelerated mice [SAM]

100%
Vorbrodt A. W., Dobrogowska D. H., Ueno M., Tarnawski M.
Folia Histochemica et Cytobiologica
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1995
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tom 33
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nr 4
2
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Impact of Curcuma longa extract on the expression level of brain transporters in in vivo model

84%
Bukowska M., Bogacz A., Wolek M., Mikolajczak P. L., Olbromski P., Kaminski A., Czerny B.
Herba Polonica
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2019
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tom 65
|
nr 1
Introduction: Blood brain barrier and multidrug resistance phenomenon are subjects of many investigations. Mainly, because of their functions in protecting the central nervous system (CNS) by blocking the delivery of toxic substances to the brain. This special function has some disadvantages, like drug delivery to the brain in neurodegenerative diseases. Objective: The aim of this study was to examine how natural and synthetic substances affect the expression levels of genes (Mdr1a, Mdr1b, Mrp1, Mrp2, Oatp1a4, Oatp1a5 and Oatp1c1) that encode transporters in the blood-brain barrier. Methods: cDNA was synthesized from total RNA isolated from rat hippocampus. The expression level of genes was determined using real-time PCR (RT-PCR) method. Results: Our findings showed that verapamil, as a synthetic substance, caused the greatest reduction of mRNA level of genes studied. The standardized extract of Curcuma longa reduced the expression level for Mrp1 and Mrp2, whereas the increase of mRNA level was observed for Mdr1b, Oatp1a5 and Oatp1c1. Conclusions: These results suggests that herbal extracts may play an important role in overcoming the blood brain barrier during pharmacotherapy
3

Permeability studies on an in vitro model of the blood-brain barrier

84%
Deli M. A., Szabo C. A., Krizbai I., Abraham C. S., Joo F.
Folia Histochemica et Cytobiologica. Supplement
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1997
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tom 35
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nr 2
4

Kinetics of a nucleoside release from lactide-caprolactone and lactide-glycolide polymers in vitro

84%
Kryczka T., Grieb P., Bero M., Kasperczyk J., Dobrzynski P.
Acta Biochimica Polonica
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2000
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tom 47
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nr 1
We assessed the rate of release of a model nucleoside (adenosine, 5%, w/w) from nine different lactide-glycolide or lactide-caprolactone polymers. The polymer discs were eluted every second day with an artificial cerebrospinal fluid at the elution rate roughly approximating the brain extracellular fluid formation rate. Adenosine in eluate samples was assayed by HPLC. Three polymers exhibited a relatively constant release of adenosine for over four weeks, resulting in micromolar concentrations of nucleoside in the eluate. This points to the neccessity of further development of polymers of this types as intracerebral nucleoside delivery systems for local treatment of brain tumors.
5
Content available remote

Myrtus communis improves cognitive impairment in renovascular hypertensive rats

67%
Cevikelli-Yakut Z.-A., Ertas B., Sen A., Koyuncuoglu T., Yegen B. C., Sener G.
Journal of Physiology and Pharmacology
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2020
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tom 71
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nr 5
6

Cerebral microvessels in rat subjected to EAE: Focus on pericytes and purinergic receptor P2X7

67%
Grygorowicz T., Lenkiewicz A., Struzynska L.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Blood-brain barrier (BBB) is a structure that maintains central nervous system (CNS) homeostasis by isolating it from the normal blood flow. In physiological conditions BBB prevents CNS penetration by blood-derived molecules and is a barrier for the immune system. BBB is built by tight junctions between endothelial cells of microvessels, pericytes, and astroglial end-feets. Pericytes are very important part of BBB showing a great impact on properties of endothelial cells and BBB tightness. In pathological conditions (i.e. inflammation) the structure of BBB is loosened and cells of the immune system have a free access to the brain and the spinal cord. That is the main mechanism of pathogenesis in both multiple sclerosis (MS) and the rodent model of the disease – experimental autoimmune encephalomyelitis (EAE). Overactivation of purinergic receptor P2X7, is a possible mechanism leading to neurodegeneration observed during the course of MS/EAE. This receptor has two distinct functions: it participates in maturation and release of proinflammatory cytokines or can polymerase to create transmembrane pores which can drive cell to death by apoptosis or necrosis. Thus, we hypothesized that overactivation of this receptor on pericytes may lead to cell damage and/or loss of the protective function towards BBB. In this study we first analyzed status of BBB which was determined by expression of claudin 5 – a marker of BBB tightness – in correlation with the expression of P2X7R in microvessels’ fractions and brain sections of rats subjected to EAE. Using immunoblots and confocal microscopic method we found negative correlation between P2X7R and claudin 5 expression which decreased significantly in all examined time points of the disease, reaching the minimum level (45% and 70% of control) at days 2 p.i. and 4 p.i., respectively. Additionally, we present the results of pericytes features and P2X7R expression in microvessels in early time after EAE induction. Condition of pericytes was visualized by immunofluorescent staining against PDGFRβ (a marker protein). Semiquantitative level of this protein was measured using Western blot analysis of brain homogenates and isolated microvessels fraction. The pattern of observed changes suggests contribution of pericyte-located P2X7R on BBB state and the involvement of this receptor into pathological mechanisms connected with development of EAE.
7

Effects of cervical sympathetic nerve stimulation on the cerebral microcirculation: possible clinical implications

67%
Passatore M., Deriu F., Roatta S., Grassi C., Micieli G.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 1
8

Peptide-based approaches to treat asthma, arthritis, other autoimmune diseases and pathologies of the central nervous system

67%
Hauff K., Zamzow C., Law W. J., De Melo J., Kennedy K., Los M.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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tom 53
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nr 4
9
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Role of prostaglandins in the stimulation of the hypothalamic-pituitary-adrenal axis by adrenergic and neurohormone systems

59%
Bugajski J.
Journal of Physiology and Pharmacology
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1996
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tom 47
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nr 4
10

Brain injury: prolonged induction of transcription factors

51%
Pennypacker K. R., Kassed C. A., Eidizadeh S., O'Callaghan J. P.
Acta Neurobiologiae Experimentalis
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2000
|
tom 60
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nr 4
A specific temporal order of events at the cellular and molecular level occurs in response to injury to the brain. Injury-compromised neurons degenerate while surviving neurons undergo neuritogenesis and synaptogenesis to establish neuronal connectivity destroyed in the injury. Several genes, such as those coding cytoskeletal proteins and growth factors, have been shown to be regulated by AP-1 and NF-kB transcription factors, two of the most studied DNA binding regulatory proteins. Our laboratory has discovered that Fos-related antigen-2 from AP-1 transcription factor family and NF-kB p65 and p50 subunits are induced long-term (days to months) in the brain after neurotoxic, excitotoxic or ischemic insult. Fos-related antigen-2 is induced in neurons in several models of injury and its elevated expression lasts days to months, corresponding to the severity. The time-course of FRA-2 induction is abbreviated with less severe insult (terminal damage) relative to the cell death, but the induction occurs during the period of regeneration and repair in both models. NF-kB p65 is basally expressed in hippocampal and cortical neurons, but is elevated in reactive astrocytes in hippocampus and entorhinal cortex starting at two days and lasting at least two weeks after kainate treatment. Neurons of the hippocampus surviving ischemic or neurotoxic injury increase expression of NF-kB p50 for at least a week after injury, suggesting a function for p50 in neuronal survival and/or repair. The extended expression of these transcription factors implies a role in the activation of genes related to repair and regeneration, such as growth factors and synaptic proteins, after injury to the CNS.
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