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  1. Article ; Online: New insights in the mode of action of (+)-erythravine and (+)-11α-hydroxy-erythravine alkaloids.

    Gelfuso, Erica A / Reis, Suelen L / Aguiar, Daiane S R / Faggion, Silmara A / Gomes, Flávia M M / Galan, Diogo T / Peigneur, Steve / Pereira, Ana M S / Mortari, Márcia R / Cunha, Alexandra O S / Tytgat, Jan / Beleboni, Renê O

    European journal of pharmacology

    2020  Volume 885, Page(s) 173390

    Abstract: Erythrinian alkaloids ((+)-erythravine and (+)-11-α-hydroxy-erythravine) have been pointed as the main responsible agents for the anticonvulsant and anxiolytic properties of Erythrina mulungu Mart ex Benth. The present work provides a new set of ... ...

    Abstract Erythrinian alkaloids ((+)-erythravine and (+)-11-α-hydroxy-erythravine) have been pointed as the main responsible agents for the anticonvulsant and anxiolytic properties of Erythrina mulungu Mart ex Benth. The present work provides a new set of information about the mode of action of these alkaloids by the use of a complementary approach of neurochemical and electrophysiological assays. We propose here that the antiepileptic and anxiolytic properties exhibited by both alkaloids appear not to be related to the inhibition of glutamate binding or GABA uptake, or even to the increase of glutamate uptake or GABA binding, as investigated here by the use of rat cortical synaptosomes. Similarly, and even in a high concentration, (+)-erythravine and (+)-11-α-hydroxy-erythravine did not modulate the main sodium and potassium channel isoforms checked by the use of voltage-clamp studies on Xenopus laevis oocytes. However, unlike (+)-11-α-hydroxy-erythravine, which presented a little effect, it was possible to observe that the (+)-erythravine alkaloid produced a significant inhibitory modulation on α
    MeSH term(s) Animals ; Anti-Anxiety Agents/pharmacology ; Anticonvulsants/pharmacology ; Cerebral Cortex/drug effects ; Cerebral Cortex/metabolism ; Erythrina/chemistry ; Glutamic Acid/metabolism ; Heterocyclic Compounds, 4 or More Rings/pharmacology ; Nicotinic Antagonists/pharmacology ; Oocytes ; Patch-Clamp Techniques ; Potassium/metabolism ; Receptors, Nicotinic/drug effects ; Sodium Channels/metabolism ; Synaptosomes/drug effects ; Synaptosomes/metabolism ; Xenopus laevis ; gamma-Aminobutyric Acid/metabolism
    Chemical Substances (+)-erythravine ; Anti-Anxiety Agents ; Anticonvulsants ; Heterocyclic Compounds, 4 or More Rings ; Nicotinic Antagonists ; Receptors, Nicotinic ; Sodium Channels ; Glutamic Acid (3KX376GY7L) ; gamma-Aminobutyric Acid (56-12-2) ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2020-07-29
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/j.ejphar.2020.173390
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: APETx4, a Novel Sea Anemone Toxin and a Modulator of the Cancer-Relevant Potassium Channel K

    Moreels, Lien / Peigneur, Steve / Galan, Diogo T / De Pauw, Edwin / Béress, Lászlo / Waelkens, Etienne / Pardo, Luis A / Quinton, Loïc / Tytgat, Jan

    Marine drugs

    2017  Volume 15, Issue 9

    Abstract: The human ether-à-go-go channel (hEag1 or ... ...

    Abstract The human ether-à-go-go channel (hEag1 or K
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor/drug effects ; Cnidarian Venoms/pharmacology ; Inhibitory Concentration 50 ; Oocytes/drug effects ; Potassium Channels, Voltage-Gated/antagonists & inhibitors ; Sea Anemones ; Toxins, Biological/pharmacology ; Xenopus
    Chemical Substances Antineoplastic Agents ; Cnidarian Venoms ; Potassium Channels, Voltage-Gated ; Toxins, Biological
    Language English
    Publishing date 2017-09-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2175190-0
    ISSN 1660-3397 ; 1660-3397
    ISSN (online) 1660-3397
    ISSN 1660-3397
    DOI 10.3390/md15090287
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Reduced mitochondrial respiration in the ischemic as well as in the remote nonischemic region in postmyocardial infarction remodeling.

    Galan, Diogo T / Bito, Virginie / Claus, Piet / Holemans, Patricia / Abi-Char, Joëlle / Nagaraju, Chandan K / Dries, Eef / Vermeulen, Kristel / Ventura-Clapier, Renée / Sipido, Karin R / Driesen, Ronald B

    American journal of physiology. Heart and circulatory physiology

    2016  Volume 311, Issue 5, Page(s) H1075–H1090

    Abstract: Scarring and remodeling of the left ventricle (LV) after myocardial infarction (MI) results in ischemic cardiomyopathy with reduced contractile function. Regional differences related to persisting ischemia may exist. We investigated the hypothesis that ... ...

    Abstract Scarring and remodeling of the left ventricle (LV) after myocardial infarction (MI) results in ischemic cardiomyopathy with reduced contractile function. Regional differences related to persisting ischemia may exist. We investigated the hypothesis that mitochondrial function and structure is altered in the myocardium adjacent to MI with reduced perfusion (MI
    MeSH term(s) AMP-Activated Protein Kinases/genetics ; Animals ; Blotting, Western ; Cardiomyopathies/diagnostic imaging ; Cardiomyopathies/etiology ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Cell Respiration ; Cicatrix ; Coronary Stenosis/complications ; Electron Transport Complex I/metabolism ; Electron Transport Complex II/metabolism ; Electron Transport Complex IV/metabolism ; Glucose Transport Proteins, Facilitative/genetics ; Glycogen/metabolism ; Magnetic Resonance Imaging ; Microscopy, Electron ; Microscopy, Fluorescence ; Mitochondria, Heart/metabolism ; Myocardial Infarction/diagnostic imaging ; Myocardial Infarction/etiology ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardial Perfusion Imaging ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/ultrastructure ; Oxygen Consumption ; RNA, Messenger/metabolism ; Real-Time Polymerase Chain Reaction ; Stroke Volume ; Sus scrofa ; Swine ; Ventricular Remodeling
    Chemical Substances Glucose Transport Proteins, Facilitative ; RNA, Messenger ; Glycogen (9005-79-2) ; Electron Transport Complex II (EC 1.3.5.1) ; Electron Transport Complex IV (EC 1.9.3.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Electron Transport Complex I (EC 7.1.1.2)
    Language English
    Publishing date 2016-09-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00945.2015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  4. Article ; Online: Cyclosporine A reduces microvascular obstruction and preserves left ventricular function deterioration following myocardial ischemia and reperfusion.

    Zalewski, Jaroslaw / Claus, Piet / Bogaert, Jan / Driessche, Nina Vanden / Driesen, Ronald B / Galan, Diogo T / Sipido, Karin R / Buszman, Piotr / Milewski, Krzysztof / Van de Werf, Frans

    Basic research in cardiology

    2015  Volume 110, Issue 2, Page(s) 18

    Abstract: Postconditioning and cyclosporine A prevent mitochondrial permeability transition pore opening providing cardioprotection during ischemia/reperfusion. Whether microvascular obstruction is affected by these interventions is largely unknown. Pigs subjected ...

    Abstract Postconditioning and cyclosporine A prevent mitochondrial permeability transition pore opening providing cardioprotection during ischemia/reperfusion. Whether microvascular obstruction is affected by these interventions is largely unknown. Pigs subjected to coronary occlusion for 1 h followed by 3 h of reperfusion were assigned to control (n = 8), postconditioning (n = 9) or cyclosporine A intravenous infusion 10-15 min before the end of ischemia (n = 8). Postconditioning was induced by 8 cycles of repeated 30-s balloon inflation and deflation. After 3 h of reperfusion magnetic resonance imaging, triphenyltetrazolium chloride/Evans blue staining and histopathology were performed. Microvascular obstruction (MVO, percentage of gadolinium-hyperenhanced area) was measured early (3 min) and late (12 min) after contrast injection. Infarct size with double staining was smaller in cyclosporine (46.2 ± 3.1%, P = 0.016) and postconditioning pigs (47.6 ± 3.9%, P = 0.008) versus controls (53.8 ± 4.1%). Late MVO was significantly reduced by cyclosporine (13.9 ± 9.6%, P = 0.047) but not postconditioning (23.6 ± 11.7%, P = 0.66) when compared with controls (32.0 ± 16.9%). Myocardial blood flow in the late MVO was improved with cyclosporine versus controls (0.30 ± 0.06 vs 0.21 ± 0.03 ml/g/min, P = 0.002) and was inversely correlated with late-MVO extent (R(2) = 0.93, P < 0.0001). Deterioration of left ventricular ejection fraction (LVEF) between baseline and 3 h of reperfusion was smaller with cyclosporine (-7.9 ± 2.4%, P = 0.008) but not postconditioning (-12.0 ± 5.5%, P = 0.22) when compared with controls (-16.4 ± 5.5%). In the three groups, infarct size (β = -0.69, P < 0.001) and late MVO (β = -0.33, P = 0.02) were independent predictors of LVEF deterioration following ischemia/reperfusion (R(2) = 0.73, P < 0.001). Despite both cyclosporine A and postconditioning reduce infarct size, only cyclosporine A infusion had a beneficial effect on microvascular damage and was associated with better preserved LV function when compared with controls.
    MeSH term(s) Animals ; Cyclosporine/pharmacology ; Disease Models, Animal ; Enzyme Inhibitors/pharmacology ; Female ; Ischemic Postconditioning/methods ; Male ; Myocardial Infarction/pathology ; Myocardial Infarction/physiopathology ; Myocardial Reperfusion Injury/pathology ; Myocardial Reperfusion Injury/physiopathology ; Myocardial Reperfusion Injury/prevention & control ; Swine
    Chemical Substances Enzyme Inhibitors ; Cyclosporine (83HN0GTJ6D)
    Language English
    Publishing date 2015-03
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-015-0475-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats.

    Oliveira, Fernando A / Guatimosim, Silvia / Castro, Carlos H / Galan, Diogo T / Lauton-Santos, Sandra / Ribeiro, Angela M / Almeida, Alvair P / Cruz, Jader S

    American journal of physiology. Heart and circulatory physiology

    2007  Volume 293, Issue 1, Page(s) H394–401

    Abstract: Extensive work has been done regarding the impact of thiamine deprivation on the nervous system. In cardiac tissue, chronic thiamine deficiency is described to cause changes in the myocardium that can be associated with arrhythmias. However, compared ... ...

    Abstract Extensive work has been done regarding the impact of thiamine deprivation on the nervous system. In cardiac tissue, chronic thiamine deficiency is described to cause changes in the myocardium that can be associated with arrhythmias. However, compared with the brain, very little is known about the effects of thiamine deficiency on the heart. Thus this study was undertaken to explore whether thiamine deprivation has a role in cardiac arrhythmogenesis. We examined hearts isolated from thiamine-deprived and control rats. We measured heart rate, diastolic and systolic tension, and contraction and relaxation rates. Whole cell voltage clamp was performed in rat isolated cardiac myocytes to measure L-type Ca(2+) current. In addition, we investigated the global intracellular calcium transients by using confocal microscopy in the line-scan mode. The hearts from thiamine-deficient rats did not degenerate into ventricular fibrillation during 30 min of reperfusion after 15 min of coronary occlusion. The antiarrhythmogenic effects were characterized by the arrhythmia severity index. Our results suggest that hearts from thiamine-deficient rats did not experience irreversible arrhythmias. There was no change in L-type Ca(2+) current density. Inactivation kinetics of this current in Ca(2+)-buffered cells was retarded in thiamine-deficient cardiac myocytes. The global Ca(2+) release was significantly reduced in thiamine-deficient cardiac myocytes. The amplitude of caffeine-releasable Ca(2+) was lower in thiamine-deficient myocytes. In summary, we have found that thiamine deprivation attenuates the incidence and severity of postischemic arrhythmias, possibly through a mechanism involving a decrease in global Ca(2+) release.
    MeSH term(s) Animals ; Arrhythmias, Cardiac/complications ; Arrhythmias, Cardiac/pathology ; Arrhythmias, Cardiac/physiopathology ; Myocardial Reperfusion Injury/complications ; Myocardial Reperfusion Injury/pathology ; Myocardial Reperfusion Injury/physiopathology ; Rats ; Rats, Wistar ; Thiamine/blood ; Thiamine Deficiency/complications ; Thiamine Deficiency/pathology ; Thiamine Deficiency/physiopathology
    Chemical Substances Thiamine (X66NSO3N35)
    Language English
    Publishing date 2007-03-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00833.2006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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