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The cardiac glycoside ouabain activates NLRP3 inflammasomes and promotes cardiac inflammation and dysfunction.
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Cardiac glycosides such as digoxin are Na+/K+-ATPase inhibitors that are widely used for the treatment of chronic heart failure and cardiac arrhythmias; however, recent epidemiological studies have suggested a relationship between digoxin treatment and increased mortality. We previously showed that
Effect of some non-steroidal anti-inflammatory drugs on ouabain-induced arrhythmias in guinea-pigs.
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1. Effects of some non-steroidal anti-inflammatory drugs on ouabain-induced arrhythmias in guinea-pigs were studied. 2. Ventricular premature beats, ventricular fibrillation and cardiac arrest were induced in pentobarbitone-anaesthetized guinea-pigs by a slow intravenous infusion of ouabain. 3.
Effects of Aspirin in Rats With Ouabain Intracerebral Treatment-Possible Involvement of Inflammatory Modulation?
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Bipolar disorder (BD) is a chronic and refractory disease with high probability of morbidity and mortality. Although epidemiological studies have established a strong association between BD and immune dysfunction, the precise etiology is still debatable, and the underpinning mechanism remains poorly
Involvement of Inflammatory Cytokines in Antiarrhythmic Effects of Clofibrate in Ouabain-Induced Arrhythmia in Isolated Rat Atria.
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Considering the cardioprotective and anti-inflammatory properties of clofibrate, the aim of the present experiment was to investigate the involvement of local and systemic inflammatory cytokines in possible antiarrhythmic effects of clofibrate in ouabain-induced arrhythmia in rats. Rats were orally
Ouabain attenuates ovalbumin-induced airway inflammation.
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OBJECTIVE
Ouabain, an Na+/K+-ATPase inhibitor hormone, presents immunomodulatory actions, including anti-inflammatory effect on acute inflammation models.
METHODS
In the present study, the effect of ouabain in a model of allergic airway inflammation induced by ovalbumin (OVA) was
Anti-inflammatory and antinociceptive activity of ouabain in mice.
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Ouabain, an inhibitor of the Na(+)/K(+)-ATPase pump, was identified as an endogenous substance of human plasma. Ouabain has been studied for its ability to interfere with various regulatory mechanisms. Despite the studies portraying the ability of ouabain to modulate the immune response, little is
Signaling function of Na,K-ATPase induced by ouabain against LPS as an inflammation model in hippocampus.
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BACKGROUND
Ouabain (OUA) is a newly recognized hormone that is synthesized in the adrenal cortex and hypothalamus. Low doses of OUA can activate a signaling pathway by interaction with Na,K-ATPase, which is protective against a number of insults. OUA has central and peripheral anti-inflammatory
Alpha 2 Na+,K+-ATPase silencing induces loss of inflammatory response and ouabain protection in glial cells.
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Ouabain (OUA) is a cardiac glycoside that binds to Na+,K+-ATPase (NKA), a conserved membrane protein that controls cell transmembrane ionic concentrations and requires ATP hydrolysis. At nM concentrations, OUA activates signaling pathways that are not related to its typical inhibitory effect on the
Much More than a Cardiotonic Steroid: Modulation of Inflammation by Ouabain.
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Since the discovery of ouabain as a cardiotonic steroid hormone present in higher mammals, research about it has progressed rapidly and several of its physiological and pharmacological effects have been described. Ouabain can behave as a stress hormone and adrenal cortex is its main source. Direct
Author Correction: Ouabain attenuates ovalbumin-induced airway inflammation.
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In the original publication, author missed to include the financial support from CAPES/PROCAD-2013. The complete funding text should read as follows.
Influence of nonsteroidal anti-inflammatory drugs on ouabain toxicity.
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Non-steroidal anti-inflammatory drugs potentiate the vasoconstrictor effects of ouabain in the dog.
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Corrigendum: Much More than a Cardiotonic Steroid: Modulation of Inflammation by Ouabain.
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[This corrects the article on p. 895 in vol. 8, PMID: 29176951.].
Human colonic (Na+ + K+)-ATPase and specific ouabain binding are not influenced by lipoxygenase products or superoxide radicals.
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The effects of lipoxygenase products (5-, 12-, 15-HETE, LTB4) and superoxide radicals on human colonic (Na+ + K+)-ATPase and specific ouabain binding were measured. No significant inhibition in concentrations up to 3 x 10(-5) M was observed. The results are discussed with regard to a possible role
Effects of ouabain on cytokine/chemokine levels in an animal model of mania.
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Bipolar disorder (BD) is a chronic and severe psychiatric disorder and despite its importance, little is known about the precise pathophysiology of this disorder. Several studies have reported that inflammation plays a role in the pathogenesis of BD and that cytokines are altered in these patients.
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