Wyniki wyszukiwania

1

Alternative methods of neuroprotection in brain ischemia

100%

Lazarewicz J.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 3

Learning of cellular and molecular mechanisms of the ischemic neuronal damage led to development of pharmacological methods of neuroprotection targeted at these mechanisms. They were effective in animal stroke models, but none of them passed clinical trials. Thus the alternative experimental neuroprotective strategies emerge. Preclinical studies demonstrated that mild hypothermia signifi cantly improves the outcome in the animal models of stroke and brain injury. This method of still unclear mechanism has been successfully used in specifi c clinical conditions and has been tested in several trials. It is hoped that moderate hypothermia soon may be introduced as an alternative method of stroke treatment. Ischemic preconditioning is a way of inducing tolerance to brain ischemia by preceding the injurious ischemia with the sub-lethal stressors like short ischemia, mild hypoxia, heating or pharmacological treatment. The exact mechanisms of activation and induction of brain tolerance to ischemia by preconditioning are not clear. Recently post-conditioning, i.e. neuroprotective effect of the post-treatment with sub-lethal stressors after injurious ischemia has been demonstrated, pointing to a therapeutic potential of such a treatment, still being tested at the preclinical level.

2

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Neuroprotective strategies using vegetal compounds in the treatment of Alzheimer’s disease

100%

Loredana S., Alin C., Radu L., Daniel T., Emil A.

International Letters of Natural Sciences

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2015

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tom 45

Lately, different therapy strategies for treating or slowing the progression of Alzheimer's disease are being analyzed. Moreover, the last two decades have seen a considerable research effort directed towards discovering the causes of Alzheimer's disease with the ultimate hope of developing safe and effective pharmacological treatments. In addition to the therapeutic strategies based on targeted drugs, the regimens will require the simultaneous application of neuroprotective drugs. Therefore, although there is currently no "cure" for Alzheimer's disease, a large number of potential therapeutic strategies emerged lately. In this small mini-review we will selectively describe some of the compounds derived from plants that could have a great potential in the treatment of various diseases, including Alzheimer's disease. In this way, there are many plant species that have been traditionally used for memory disorders. The differentiated results and powerful activity of these extracts are making these neuroprotective strategies to be somehow plausible for the treatment of Alzheimer's disease. In addition, these plants can be examined in order to isolate and identify their active ingredients and this can serve as a starting point to find safer and more effective agents for therapeutic use. On thing is certain: as the effective treatment options are limited, there is a demand for new drugs. Thus, plant extracts or vegetal compounds could represent an important part in this equation.

3

NG2 expressing cells in hippocampal cultures survive neurotoxic insult and retain the ability to divide

100%

Dzwonek K.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 2

4

Gonadotropins and Alzheimer's disease: the link between estrogen replacement therapy and neuroprotection

100%

Webber K. M., Bowen R., Casadesus G., Perry G., Atwood C. S., Smith M. A.

Acta Neurobiologiae Experimentalis

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2004

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tom 64

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nr 1

5

p-ERK involvement in the neuroprotection exerted by ischemic preconditioning in rat hippocampus subjected to four vessel occlusion

84%

Kovalska M., Kovalska L., Mikuskova K., Tatarkova Z., Lehotsky J.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 6

6

Potassium channels in brain mitochondria

84%

Bednarczyk P.

Acta Biochimica Polonica

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2009

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tom 56

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nr 3

385-392

Potassium channels are the most widely distributed class of ion channels. These channels are transmembrane proteins known to play important roles in both normal and pathophysiological functions in all cell types. Various potassium channels are recognised as potential therapeutic targets in the treatment of Parkinson's disease, Alzheimer's disease, brain/spinal cord ischaemia and sepsis. In addition to their importance as therapeutic targets, certain potassium channels are known for their beneficial roles in anaesthesia, cardioprotection and neuroprotection. Some types of potassium channels present in the plasma membrane of various cells have been found in the inner mitochondrial membrane as well. Potassium channels have been proposed to regulate mitochondrial membrane potential, respiration, matrix volume and Ca2+ ion homeostasis. It has been proposed that mitochondrial potassium channels mediate ischaemic preconditioning in various tissues. However, the specificity of a pharmacological agents and the mechanisms underlying their effects on ischaemic preconditioning remain controversial. The following potassium channels from various tissues have been identified in the inner mitochondrial membrane: ATP-regulated (mitoKATP) channel, large conductance Ca2+-regulated (mitoBKCa) channel, intermediate conductance Ca2+-regulated (mitoIKCa) channel, voltage-gated (mitoKv1.3 type) channel, and twin-pore domain (mitoTASK-3) channel. It has been shown that increased potassium flux into brain mitochondria induced by either the mitoKATP channel or mitoBKCa channel affects the beneficial effects on neuronal cell survival under pathological conditions. Recently, differential distribution of mitoBKCa channels has been observed in neuronal mitochondria. These findings may suggest a neuroprotective role for the mitoBKCa channel in specific brain structures. This minireview summarises current data on brain mitochondrial potassium channels and the efforts to identify their molecular correlates.

7

Essentiality and toxicity of vanadium supplements in health and pathology

84%

Gruzewska K., Michno A., Pawelczyk T., Bielarczyk H.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 5

8

Signals mediating Klotho-induced neuroprotection in hippocampal neuronal cells

84%

Cheng M.-F., Chen L.-J., Niu H.-S., Yang T.-T., Lin K.-C., Cheng J.-T.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr 1

The erythropoietin (Epo) receptor (EpoR) is expressed in the brain and was shown to have neuroprotective effects against brain damage in animal models. A recent study indicated that EpoR and its activity are the downstream effectors of Klotho for cytoprotection in the kidney. Thus, we propose that Klotho can stimulate the expression of EpoR in neuronal cells to enhance Epo-mediated protection. H19-7 hippocampal neuronal cells were treated with recombinant Klotho. In H19-7 cells, Klotho increased the expression of both the EpoR protein and mRNA. Klotho also enhanced the transcription activity of the EpoR promoter in H19-7 cells. Moreover, Klotho augmented the Epo-triggered phosphorylation of Jak2 and Stat5 and protected H19-7 cells from hydrogen peroxide cytotoxicity. The silencing of EpoR abolished the protective effect of Klotho against peroxide-induced cytotoxicity. Finally, the silencing of GATA1 diminished the Klotho-induced increase in EpoR protein and mRNA expression as well as its promoter activity. In conclusion, Klotho increased EpoR expression in neuronal cells through GATA1, thereby enabling EpoR to function as a cytoprotective protein against oxidative injury.

9

Leukemia inhibitory factor inhibits the proliferation of primary rat astrocytes induced by oxygen-glucose deprivation

84%

Fan Y.-Y., Zhang J.-M., Wang H., Liu X.-Y., Yang F.-H.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 4

Leukemia inhibitory factor (LIF) is a neuroprotective cytokine that is necessary for the normal development of astrocytes. Oxygen-glucose deprivation (OGD) can induce astrocyte proliferation by increasing hypoxia-inducible factor alpha (HIF- 1a) and vascular endothelial growth factor (VEGF). Here, we studied whether LIF affects the proliferation of cultured primary rat astrocytes under OGD conditions by measuring EdU incorporation into astrocyte DNA and the expression of proliferating cell nuclear antigen (PCNA) mRNA and protein. Our findings show that low concentrations of LIF (5 and 10 ng/mL) significantly decreased EdU incorporation and downregulated the expression of PCNA mRNA and PCNA protein in astrocytes subjected to OGD. A low concentration of LIF (10 ng/mL) clearly inhibited astrocyte proliferation induced by OGD, while a higher concentration (50 ng/mL) had no effect. To investigate the mechanism of this inhibition by LIF (10 ng/ mL), the expression of 3 related genes (LIF receptor, HIF-1a, and VEGF) was assessed using real-time PCR; VEGF protein expression was measured by Western blot. Our results indicate that LIFR mRNA was downregulated in astrocytes subjected to OGD. Interestingly, treatment with LIF further reduced LIFR mRNA expression in these cells. LIF treatment also decreased the expression of HIF-1a mRNA, VEGF mRNA, and VEGF protein induced by OGD. Low concentrations of LIF were observed to inhibit astrocyte proliferation induced by OGD.

10

Molecular hydrogen affords neuroprotection in a translational piglet model of hypoxic-ischemic encephalopathy

84%

Nemeth J., Toth-Szuki V., Varga V., Kovacs V., Remzso G., Domoki F.

Journal of Physiology and Pharmacology

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2016

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tom 67

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nr 5

11

Carboxyl terminal fragment of beta-amyloid precursor protein: electrophysiological effects and cellular toxicity

84%

Fraser S. P., Bryan A. A., Diss J. K. J., Kim J. H., Kim S. H., Suh Y. H., Djamgoz M. B. A.

Cellular and Molecular Biology Letters

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1997

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tom 02

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nr 2

Alzheimer's disease (AD) is characterized by deposition of β-amyloid (Aβ) in areas of the brain. Aβ is a metabolic fragment of the β-amyloid precursor protein (βAPP). Genetic evidence has linked βAPP to AD, and there is increasing evidence that fragments from βAPP are neurotoxic. Aβ, the main research focus, has been shown to induce depolarizing ion channel activity. Involvement of other cleaved products from βAPP are less clear. We have investigated the 105 amino acid C-terminal peptide (CT105) (containing the full sequence Aβ), an alternative fragment linked with cellular toxicity. CT105 induced non-selective ionic currents in Xenopus oocytes (a model cell used in cell signalling studies) and was toxic to oocytes and mammalian cortical neurones. These results suggest possible involvement of CT105 in inducing the neural toxicity characteristic of AD.

12

Changes of Ca 2-calmodulin-dependent protein kinase-II after transient ischemia in gerbil hippocampus

84%

Zalewska T., Zablocka B., Domanska-Janik K.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 1

13

Glutamate excitotoxicity in transient global cerebral ischemia

84%

Paschen W.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 1

14

Brain preconditioning and obstructive sleep apnea syndrome

84%

Brzecka A.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 2

15

Investigations of hippocampal astrocytes in lipopolysaccharide-preconditioned rats in the pilocarpine model of epilepsy

67%

Jaworska-Adamu J., Dmowska M., Cybulska R., Krawczyk A., Pawlikowska-Pawlega B.

Folia Histochemica et Cytobiologica

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2011

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tom 49

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nr 2

16

Levetiracetam protects hippocampal neurons in culture against hypoxia-induced injury

67%

Sendrowski K., Bockowski L., Sobaniec W., Ilendo E., Jaworowska B., Smigielska-Kuzia J.

Folia Histochemica et Cytobiologica

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2011

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tom 49

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nr 1

17

Impact of raloxifene and 3,3’-diindolylmethane on neuronal cells exposed to hypoxia

67%

Rzemieniec J., Litwa E., Lason W., Kajta M.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

During the neonatal period of life, hypoxia appears as a major risk factor which may result in complex cerebral dysfunctions like cerebral palsy or seizure disabilities. Natural neuroprotection against hypoxia-induced injury in females is considered to be due to the effects of circulating ovarian hormones, which are lost after ovariectomy or reproductive senescence. Although anti-hypoxic effects of estrogen have been documented, its clinical use has certain limitations. Selective estrogen receptor modulators (SERMs) and selective aryl hydrocarbon receptor modulators (SAhRs) may act as receptor agonists or antagonists in a tissue-specific manner, thus representing a novel approach for the treatment or the prevention of various types of neural degeneration and seizures. In this study we evaluated the mechanism of action of raloxifene and 3,3’-diindolylmethane (DIM) in response to hypoxia in mouse embryonic neuronal cells in primary cultures. Raloxifene is known to bind to estrogen receptors with SERM properties, whereas (DIM) exhibits properties of SAhRs. In our study, hypoxic conditions (5% CO2/95% nitrogen) induced caspase-3 activity and lactate dehydrogenase (LDH) release in the hippocampal cell cultures. Raloxifene and DIM inhibited the hypoxia-induced LDH release by 10–51% and 9–61%, respectively. DIM inhibited also the hypoxia-induced caspase-3 activity by 2–18%, but raloxifene did not affect the hypoxia-induced apoptotic parameter. In our model of hypoxia, estrogen receptor alpha (ER alpha) antagonist MPP (0.01 µM) did not reverse raloxifene-mediated neuroprotection. However, a high-affinity estrogen receptor beta (ER beta) antagonist, PHTPP (0.01 μM), and G-protein coupled receptor 30 antagonist (GPR30), G-15 (0.01 µM), enhanced the neuroprotective effects of raloxifene, which point to neurotoxic potential of ER beta and GPR30 activation in hypoxia. Selective antagonist of aryl hydrocarbon receptors (AhR) alpha-naphthoflavone (1 µM) did not influence neuroprotective action of DIM, thus suggesting AhR-independent effect. These data demonstrated strong neuroprotective potential of raloxifene and DIM which may represent novel therapeutic tools for brain exposed to hypoxic insults. This study was supported by the Polish National Center of Science grant No 2011/01/N/NZ3/04786

18

Calcium-binding proteins immunoreactivity during ontogenesis of the limbic structures in the guinea pig

67%

Robak A.

Acta Biologica Cracoviensia. Series Botanica. Supplement

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2014

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tom 56

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nr 1

19

Effects of MK-801 and ganglioside GM1 on postischemic prostanoid release and hippocampal lesion in gerbil brain

67%

Lazarewicz J. W., Salinska E., Speina E., Gadamski R.

Acta Neurobiologiae Experimentalis

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1994

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tom 54

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nr 4

20

Neuroprotective effect of ACTH [4-9] in degeneration of hippocampal nerve cells caused by dexamethasone: morphological, immunocytochemical and ultrastructural studies

67%

Sekita-Krzak J., Zebrowska-Lupina I., Czerny K., Stepniewska M., Wrobel A.

Acta Neurobiologiae Experimentalis

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2003

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tom 63

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nr 1

Ograniczanie wyników

Alternative methods of neuroprotection in brain ischemia

Neuroprotective strategies using vegetal compounds in the treatment of Alzheimer’s disease

NG2 expressing cells in hippocampal cultures survive neurotoxic insult and retain the ability to divide

Gonadotropins and Alzheimer's disease: the link between estrogen replacement therapy and neuroprotection

p-ERK involvement in the neuroprotection exerted by ischemic preconditioning in rat hippocampus subjected to four vessel occlusion

Potassium channels in brain mitochondria

Essentiality and toxicity of vanadium supplements in health and pathology

Signals mediating Klotho-induced neuroprotection in hippocampal neuronal cells

Leukemia inhibitory factor inhibits the proliferation of primary rat astrocytes induced by oxygen-glucose deprivation

Molecular hydrogen affords neuroprotection in a translational piglet model of hypoxic-ischemic encephalopathy

Carboxyl terminal fragment of beta-amyloid precursor protein: electrophysiological effects and cellular toxicity

Changes of Ca 2-calmodulin-dependent protein kinase-II after transient ischemia in gerbil hippocampus

Glutamate excitotoxicity in transient global cerebral ischemia

Brain preconditioning and obstructive sleep apnea syndrome

Investigations of hippocampal astrocytes in lipopolysaccharide-preconditioned rats in the pilocarpine model of epilepsy

Levetiracetam protects hippocampal neurons in culture against hypoxia-induced injury

Impact of raloxifene and 3,3’-diindolylmethane on neuronal cells exposed to hypoxia

Calcium-binding proteins immunoreactivity during ontogenesis of the limbic structures in the guinea pig

Effects of MK-801 and ganglioside GM1 on postischemic prostanoid release and hippocampal lesion in gerbil brain

Neuroprotective effect of ACTH [4-9] in degeneration of hippocampal nerve cells caused by dexamethasone: morphological, immunocytochemical and ultrastructural studies