Wyniki wyszukiwania - Biblioteka Nauki

1

Granulocyte colony-stimulating factor potential use in the treatment of children with cerebral palsy

100%

Paszko-Patej G. , Sienkiewicz D. , Okurowska-Zawada B. , Kułak W.

Progress in Health Sciences

|

2017

|

tom 7(1)

187-192

EN

Granulocyte colony-stimulating factor (G-CSF) is a glycoprotein that stimulates the bone marrow to produce granulocytes and stem cells and release them into the blood. Recent studies demonstrated the presence of CSF-receptor (G-CSFR) system in the brain and spinal cord, and their roles in neuroprotection and neural tissue repair, as well as improvement in functional recovery. G-CSF exerts neuroprotective actions through the inhibition of apoptosis and inflammation, and the stimulation of neurogenesis. This review highlights recent studies on the potential use of G-CSF in cerebral palsy.

2

Natural and Synthetic Coumarins and their Pharmacological Activity

100%

Tomasz Kubrak T. , Rafał Podgórski R. , Monika Sompor M.

European Journal of Clinical and Experimental Medicine

|

2017

|

nr 2

169-175

EN

Coumarins are a structurally diverse group of natural substances derives from plants that display a host of bioactivities. In this paper, we will introduce the reader to coumarins and their applications as medicinal substances. The great diversity in courmarin structure will be discussed along with their extensive use as pharmaceutical agents. Coumarins display a wide range of antimicrobial activity and applications of coumarins as antifungal and antiviral agents will be addressed. Other properties of coumarins such as their role in neuroprotection, anticancer, and as antioxidants will also be reviewed.

3

Multiple sclerosis – new therapeutic directions

88%

Łowiec P. , Trzonkowski P. , Chwojnicki K.

European Journal of Translational and Clinical Medicine

|

2019

|

tom 2

|

nr 1

7-22

EN

Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease which affects the central nervous system. Currently, there are numerous disease-modifying therapies for this condition. Most of them address the inflammatory aspects of the disease and are most effective in the relapsing-remitting stages of multiple sclerosis. However, none of them can completely stop the progression of MS and they are usually associated with adverse effects. There is an ongoing search for novel approaches that involve different modes of action. Here, we discuss examples of new immunomodulating agents such as antigen-specific therapies, neuroprotectants, regenerative strategies and gut microbiota modification.

4

Multiple sclerosis – new therapeutic directions

88%

Łowiec P. , Trzonkowski P. , Chwojnicki K.

European Journal of Translational and Clinical Medicine

|

2019

|

tom 2

|

nr 1

7-22

EN

Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease which affects the central nervous system. Currently, there are numerous disease-modifying therapies for this condition. Most of them address the inflammatory aspects of the disease and are most effective in the relapsing-remitting stages of multiple sclerosis. However, none of them can completely stop the progression of MS and they are usually associated with adverse effects. There is an ongoing search for novel approaches that involve different modes of action. Here, we discuss examples of new immunomodulating agents such as antigen-specific therapies, neuroprotectants, regenerative strategies and gut microbiota modification.

5

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

75%

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

International Letters of Natural Sciences

|

2015

|

tom 45

EN

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.

6

Selected classical and novel antiepileptic drugs – mechanisms of action, neuroprotection, and effectiveness in epileptic and non-epileptic conditions

75%

Chrościńska-Krawczyk M. , Wałek M. , Tylus B. , Czuczwar S. J.

|

nr 1

37-50

EN

Introduction. One of the most common neurological disorders is epilepsy, characterised by recurrent spontaneus seizures. Although not fully efficient in ca 30% of patients, pharmacologic treatment of epilepsy plays an important therapeutic approach not only against epilepsy. Aim. To provide data on the mechanism of action, activity and neuroprotective efficacy in experimental conditions, clinical efficacy against epilepsy and non-epileptic diseases of major, classical and newer antiepileptic drugs (AEDs – lamotrigine, topiramate, levetiracetam, valproate and carbamazepine). Methods. A literature search for publications written in English, preferably published within a period of the last fifteen years, using the key words listed below. Review. The majority of AEDs possess more than one mechanism of action. They exert their effect by acting on various receptors (different types of glutamatergic and mainly GABAA receptors), neurotransmitters (mainly glutamate or GABA) and voltage-gated ion channels (sodium or calcium ion channels). All reviewed AEDs possess neuroprotective activity, the weakest being carbamazepine. Apart from epilepsy, AEDs may be also used in the pharmacotherapy of migraine, neuropathic pain, spasticity, psychiatric disorders and Parkinsons's or Alzheimer's diseases. Conclusions. As highlighted above, around 30% of epileptic patients do not substantially benefit from AEDs. It is possible that rational combinations of AEDs, based upon experimental studies, could improve this outcome. The neuroprotective effects of AEDs may point to their disease-modifying activity.

7

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

75%

Dzwonek K.

Acta Neurobiologiae Experimentalis

|

2005

|

tom 65

|

nr 2

8

Mechanizm działania jonów litu w ośrodkowym układzie nerwowym

63%

Gawlik O. , Rabe-Jabłońska J.

|

nr 4

211-217

EN

The aim of this paper is to present current views on proved and possible mechanisms of action of lithium ion in the central nervous system. In spite of the long history of lithium usage in medicine, its mechanism of therapeutic action still has not been fully understood and is being under intensive researches. There have been proposed many hypotheses for this mechanism. They include: the ions (mainly sodium) transport modulation and neurotransmitters, especially monoamines, signalling modulation (regulation of dopaminergic and noradrenergic neurotransmission and stimulation of serotonin secretion); the interference with the secondary messenger systems: mainly phosphatydyloinositol (PI) signalling pathway (inositol mono- and polyphosphatase inhibition) and also cyclic adenosine monophosphate (cAMP) system; other intracellular messengers (like G proteins, protein kinase C or calcium ion); many neuroprotection effects: increasing expression of neuroprotective factors (bcl-2, BAG-1, BDNF and others), the caspases cascade leading to apoptosis inhibition, glycogen synthase kinase 3 subunit (GSK-3b inhibition – this is one of the most important targets for lithium ion in the cell), influence on neurogenesis, reduction of glutaminergic neurotransmission or possible lithium ion action as an antioxidant factor; long-term treatment with lithium salts regulates genes expression in neurons. Understanding the mechanism of lithium action would help researchers to advance not only in finding better drugs for the disease treatment by also in understanding the disease itself.

PL

Celem niniejszego opracowania jest przedstawienie obecnej wiedzy na temat udowodnionych i możliwych mechanizmów działania jonów litu w ośrodkowym układzie nerwowym. Pomimo długiej historii stosowania litu w medycynie ów mechanizm jego działań terapeutycznych wciąż nie został w pełni zrozumiany i podlega intensywnym badaniom. Zaproponowano wiele hipotez odnoszących się do tego działania, wśród których znajdują się: modulacja transportu jonów (głównie sodu) i modulacja neuroprzekaźnictwa, szczególnie w obrębie monoamin (regulacja przekaźnictwa dopaminergicznego i noradrenergicznego oraz stymulacja wydzielania serotoniny); oddziaływanie na układy wtórnych przekaźników: głównie ścieżkę fosfatydyloinozytolu (PI) (hamowanie aktywności mono- i polifosfatazy inozytolu), a także układ cyklicznego adenozynomonofosforanu (cAMP); wpływ na inne systemy przekaźnictwa wewnątrzkomórkowego (takie jak białka G, kinaza białkowa C czy jony wapnia); wiele efektów neuroprotekcyjnych: nasilenie ekspresji czynników neuroprotekcyjnych (bcl-2, BAG-1, BDNF i in.), hamowanie szlaku kaspaz prowadzącego do apoptozy, hamowanie aktywności podjednostki kinazy fosfatazy glikogenu (GSK-3b – jest to jeden z głównych punktów uchwytu dla jonów litu w komórce), wpływ na neurogenezę, redukcja przekaźnictwa glutaminianergicznego oraz możliwa rola jonów litu jako czynnika antyoksydacyjnego; długoterminowe leczenie solami litu reguluje z kolei ekspresję genów w komórkach nerwowych. Zrozumienie mechanizmów działania jonów litu może pomóc nie tylko w opracowaniu nowych lepszych leków, lecz także w dokładniejszym zrozumieniu istoty chorób układu nerwowego, w których terapii stosujemy lit.

9

Potassium channels in brain mitochondria

63%

Bednarczyk P.

Acta Biochimica Polonica

|

2009

|

tom 56

|

nr 3

385-392

EN

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.

10

Czy pochodne nukleozydów i nukleotydów mogą w przyszłości stać się skutecznymi lekami przeciwpadaczkowymi?

63%

Cieślak M. , Komoszyński M.

Aktualności Neurologiczne

|

2010

|

tom 10

|

nr 4

206-212

EN

Many examples of experimental epilepsy show that epileptic seizures occur due to release of stimulatory neurotransmitters into intracellular spaces. In CNS adenosine suppresses exocytosis of glutamate and asparginate but guanosine increases the reverse uptake of glutamate by astrocytes and thus lowers it concentration outside the cell. In this process both nucleosides participate in suppressing the epileptic seizures. By decreasing concentration of ectoadenosine and ectoguanosine outside the cell, that compounds can protect neurons from cellular degeneration. It was shown in many animal models for experimental epilepsy that adenosine A1 and A2A receptors were involved in the process of stopping the seizures. Moreover, some of the conventional anti-epileptic drugs reveal enhance their therapeutic abilities by interactions with the adenosine receptors, being either agonists or antagonists. These interactions modulate the activity of receptors and consequently regulate the neuroprotection processes. Some agonists of adenosine receptors increase the epileptic episodes reaction to those compounds. Anti-episode action of adenosine and guanosine as well as agonists and antagonists of nucleoside receptors indicate the possibility of applying the knowledge about these processes towards production of new anti-epileptic medication. Successful anti-epileptic medication may be based on compounds that have the ability to increase the concentration of ectoadenosine i.e; adenosine deaminase inhibitors, adenosine kinase inhibitors or compounds with ability to suppress reverse uptake of nucleosides. Another method to increase the concentration of extracellular adenosine is to increase the activity of 5’-nucleotidase. That in effect will increase the amount of ectoadenosine by degradation of ectoAMP. There are very promising results revealed that oral administration of guanosine and GMP as well as guanosine by itself given intraperitoneally and intraventricularly what halted epileptic seizures caused by quinolinic acid which is a glutamate agonist.

PL

Napady drgawkowe są wynikiem uwalniania neurotransmiterów pobudzających do przestrzeni pozakomórkowej. W ośrodkowym układzie nerwowym ektoadenozyna hamuje egzocytozę glutaminianu i asparaginianu, natomiast ektoguanozyna, zwiększając wychwyt zwrotny glutaminianu przez astrocyty, obniża jego stężenie poza komórką. W ten sposób oba nukleozydy uczestniczą w hamowaniu napadu drgawkowego. Nukleozydy te, obniżając stężenie powyższych neurotransmiterów poza komórką, chronią neurony przed śmiercią, pełnią więc funkcję neuroprotekcyjną. W różnych modelach zwierzęcych padaczek eksperymentalnych wykazano, że w przerwaniu napadu drgawkowego uczestniczą receptory adenozynowe A1 i A2A. Ma miejsce współdziałanie leków przeciwpadaczkowych i receptorów adenozynowych, bowiem niektóre z nich, takie jak karbamazepina, działają za pośrednictwem receptorów adenozynowych A1, a niektórzy agoniści receptorów A1 potęgują działanie przeciwdrgawkowe tych leków. Przeciwdrgawkowe działanie adenozyny i guanozyny oraz agonistów i antagonistów receptorów nukleozydowych wskazuje na możliwość wykorzystania wiedzy o tych procesach w projektowaniu nowych leków przeciwpadaczkowych. Skutecznymi lekami przeciwdrgawkowymi mogą okazać się związki zwiększające stężenie ektoadenozyny, takie jak: inhibitory deaminazy adenozyny, kinazy adenozynowej oraz związki hamujące wychwyt zwrotny nukleozydów. Innym sposobem zwiększenia stężenia pozakomórkowej adenozyny jest wzrost aktywności 5’-nukleotydazy powiększającej pulę ektoadenozyny przez degradację ektoAMP. Obiecujące są również rezultaty doustnego podania guanozyny i GMP, a także samej guanozyny podanej dokomorowo i dootrzewnowo, które powodowało przerywanie drgawek wywoływanych przez agonistę glutaminianu – kwas chinolinowy.

11

Czy pochodne nukleozydów i nukleotydów mogą w przyszłości stać się skutecznymi lekami przeciwpadaczkowymi?

63%

Ciślak M. , Komoszyński M.

Aktualności Neurologiczne

|

2006

|

tom 6

|

nr 2

124-130

EN

Many examples of experimental epilepsy show that epileptic seizures occur due to release of stimulatory neurotransmitters into intracellular spaces. In CNS adenosine suppresses exocytosis of glutamate and asparginate but guanosine increases the reverse uptake of glutamate by astrocytes and thus lowers it concentration outside the cell. In this process both nucleosides participate in suppressing the epileptic seizures. By decreasing concentration of ectoadenosine and ectoguanosine outside the cell, that compounds can protect neurons from cellular degeneration. It was shown in many animal models for experimental epilepsy that adenosine A1 and A2A receptors were involved in the process of stopping the seizures. Moreover, some of the conventional anti-epileptic drugs reveal enhance their therapeutic abilities by interactions with the adenosine receptors, being either agonists or antagonists. These interactions modulate the activity of receptors and consequently regulate the neuroprotection processes. Some agonists of adenosine receptors increase the epileptic episodes reaction to those compounds. Anti-episode action of adenosine and guanosine as well as agonists and antagonists of nucleoside receptors indicate the possibility of applying the knowledge about these processes towards production of new anti-epileptic medication. Successful anti-epileptic medication may be based on compounds that have the ability to increase the concentration of ectoadenosine i.e. adenosine deaminase inhibitors, adenosine kinase inhibitors or compounds with ability to suppress reverse uptake of nucleosides. Another method to increase the concentration of extracellular adenosine is to increase the activity of 5’-nucleotidase. That in effect will increase the amount of ectoadenosine by degradation of ecto-AMP. There are very promising results revealed that oral administration of guanosine and GMP as well as guanosine by itself given intraperitoneally and intraventricularly what halted epileptic seizures caused by quinolinic acid which is a glutamate agonist.

PL

Napady drgawkowe są wynikiem uwalniania neurotransmiterów pobudzających do przestrzeni pozakomórkowej. W ośrodkowym układzie nerwowym ektoadenozyna hamuje egzocytozę glutaminianu i asparaginianu, natomiast ektoguanozyna, zwiększając wychwyt zwrotny glutaminianu przez astrocyty, obniża jego stężenie poza komórką. W ten sposób oba nukleozydy uczestniczą w hamowaniu napadu drgawkowego. Nukleozydy te, obniżając stężenie powyższych neurotransmiterów poza komórką, chronią neurony przed śmiercią, pełnią więc funkcję neuroprotekcyjną. W różnych modelach zwierzęcych padaczek eksperymentalnych wykazano, że w przerwaniu napadu drgawkowego uczestniczą receptory adenozynowe A1 i A2A. Ma miejsce współdziałanie leków przeciwpadaczkowych i receptorów adenozynowych, bowiem niektóre z nich, takie jak karbamazepina, działają za pośrednictwem receptorów adenozynowych A1, a niektórzy agoniści receptorów A1 potęgują działanie przeciwdrgawkowe tych leków. Przeciwdrgawkowe działanie adenozyny i guanozyny oraz agonistów i antagonistów receptorów nukleozydowych wskazuje na możliwość wykorzystania wiedzy o tych procesach w projektowaniu nowych leków przeciwpadaczkowych. Skutecznymi lekami przeciwdrgawkowymi mogą okazać się związki zwiększające stężenie ektoadenozyny, takie jak: inhibitory deaminazy adenozyny, kinazy adenozynowej oraz związki hamujące wychwyt zwrotny nukleozydów. Innym sposobem zwiększenia stężenia pozakomórkowej adenozyny jest wzrost aktywności 5’-nukleotydazy powiększającej pulę ektoadenozyny przez degradację ektoAMP. Obiecujące są również rezultaty doustnego podania guanozyny i GMP, a także samej guanozyny podanej dokomorowo i dootrzewnowo, które powodowało przerywanie drgawek wywoływanych przez agonistę glutaminianu – kwas chinolinowy.

12

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

63%

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

|

nr 5

13

Signals mediating Klotho-induced neuroprotection in hippocampal neuronal cells

63%

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

Acta Neurobiologiae Experimentalis

|

2015

|

tom 75

|

nr 1

EN

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.

14

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

63%

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

|

tom 73

|

nr 4

EN

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.

15

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

63%

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

|

nr 6

16

Essentiality and toxicity of vanadium supplements in health and pathology

63%

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

Journal of Physiology and Pharmacology

|

2014

|

tom 65

|

nr 5

17

Characteristics of ketogenic diet and its therapeutic properties in central nervous system disorders

63%

Liśkiewicz A. , Jędrzejowska-Szypułka H. , Lewin-Kowalik J.

Annales Academiae Medicae Silesiensis

|

2012

|

tom 66

|

nr 6

66-76

EN

A fat-rich and low-carbohydrate ketogenic diet has been successfully used in epilepsy treatment in children and adults for many years. Lately, advances have been made in the use of ketogenics as therapy for other disorders such the tuberous sclerosis complex, brain tumors and neurodegenerative diseases: Alzheimer’s disease and Parkinson’s disease. Many studies have also shown its neuroprotective abilities. This neuroprotection is connected with the molecular mechanisms of a ketogenic diet and ketone metabolism. This review shows how a ketogenic diet induces ketosis, how it works and how the molecular mechanisms of a ketogenic diet may be used in the therapy of central nervous system disorders.

PL

Wysokotłuszczowa, niskowęglowodanowa dieta ketogenna jest terapią, która od wielu lat z sukcesem jest stosowana u dzieci i dorosłych w leczeniu epilepsji. Późniejsze badania pozwoliły na rozszerzenie poszukiwań jej terapeutycznego zastosowania o stwardnienie guzowate, guzy mózgu i schorzenia neurodegeneracyjne, jak choroba Alzheimera i choroba Parkinsona. Wiele badań wykazało również neuroprotekcyjne właściwości tej terapii. Indukowanie neuroprotekcji jest związane z molekularnymi mechanizmami działania diety ketogennej i metabolizmem ciał ketonowych. Niniejsza praca opisuje działanie diety ketogennej oraz jej mechanizmy molekularne, które mogą być wykorzystywane w terapii chorób centralnego układu nerwowego.

18

Neuroprotekcyjne właściwości związków pochodzenia roślinnego: triterpeny pentacykliczne

63%

Orłowska-Majdak M.

|

2014

|

tom 14

|

nr 4

284-289

EN

The brain is a structure of great variability during the ontogenetic human life. In the first period of life, changes in its structure and activities are due to the processes of development and maturation. Then, due to the remarkable synaptic plasticity, individual brain centres adapt to the requirements of the environment in which the man lives, and his lifestyle. After the age of 40 years, apoptosis, the process of programmed cell death of neurons begins. In a state of disease, the process of necrosis or aponecrosis may cause additional destruction of neurons. The process of neurogenesis based on local or transplanted brain stem cells has a repairing effect in the damaged structures, but may be also associated with psychiatric and neurological diseases. Underlying processes of neuroprotection include antioxidant, anti-inflammatory, anti-apoptotic processes and antidestructive action of Ca. Phytotherapy based on compounds of plant origin has been found to have a supporting function in neuroprotection. In recent years, particular attention is paid to neuroprotective properties of pentacyclic triterpenes and their derivatives. The article presents neuroprotective properties of ursolic, oleanolic, maslinic, asiatic, betulinic, boswellic acid and triterpene saponins from Bupleurum and Panax ginseng. Ginseng saponins additionally increase neurogenesis in the brain. The possibility of using these triterpene compounds in the treatment of many neurological and psychiatric diseases has been suggested. However, it should be pointed out that the direction of their action may depend on the dosage, they may have a different effect on various types of neurons, and they can interact with other drugs used simultaneously. Most of the experiments using triterpenes were performed on animals or cell cultures. Further studies in humans are required to further determine triterpene effect in humans.

PL

Ludzki mózg to struktura wykazująca ogromną zmienność w ciągu życia osobniczego. W pierwszym okresie zmiany budowy i czynności spowodowane są procesami rozwoju i dojrzewania. Następnie, dzięki niezwykłej plastyczności synaptycznej, poszczególne ośrodki mózgu przystosowują się do wymagań środowiska, w jakim człowiek funkcjonuje, i do stylu jego życia. Po 40. roku życia włącza się proces zaprogramowanej śmierci neuronów, czyli apoptozy, a w stanie choroby neurony mogą ginąć w procesie nekrozy lub aponekrozy. Neurogeneza na bazie miejscowych albo transplantowanych komórek macierzystych mózgu pełni funkcję naprawczą w powstałych uszkodzeniach, ale może także mieć związek z chorobami psychicznymi i neurologicznymi. U podstaw neuroprotekcji leżą procesy antyoksydacyjne, przeciwzapalne, antyapoptotyczne i przeciwdziałające destrukcyjnemu działaniu jonów wapnia. Wspierającą funkcję w działaniu neuroprotekcyjnym mogą mieć związki pochodzenia roślinnego, podawane w ramach fitoterapii. W ostatnich latach zwrócono uwagę na neuroprotekcyjne właściwości pentacyklicznych triterpenów i ich pochodnych. W pracy omówiono właściwości neuroprotekcyjne kwasu ursolowego, oleanolowego, maslinowego, asjatowego, betulinowego, bosweliowego oraz saponin triterpenowych pozyskiwanych z roślin Bupleurum i Panax ginseng. Saponiny ginseng dodatkowo nasilają neurogenezę w mózgu. Sugeruje się potencjał stosowania wymienionych związków w terapii wielu chorób neurologicznych i psychicznych – z kilkoma zastrzeżeniami: 1) kierunek działania może zależeć od dawki; 2) związki te mogą różnie działać na neurony różnych rodzajów; 3) mogą istnieć niekorzystne interakcje z innymi lekami stosowanymi równocześnie. Większość doświadczeń z użyciem triterpenów wykonano na zwierzętach bądź w hodowlach komórkowych, zagadnienie wymaga więc dalszych badań na ludziach.

19

Brain preconditioning and obstructive sleep apnea syndrome

63%

Brzecka A.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 2

20

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

63%

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

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nr 1