ouabain/necroză

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Na+/K+ pump and endothelial cell survival: [Na+]i/[K+]i-independent necrosis triggered by ouabain, and protection against apoptosis mediated by elevation of [Na+]i.

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Recent studies have demonstrated the tissue-specific effect of Na+/K+ pump inhibition by ouabain and other cardiac glycosides on cell viability. The vascular endothelium is an initial target of cardiac glycosides employed for the management of congestive heart failure as well as circulating

Ionic mechanism of ouabain-induced concurrent apoptosis and necrosis in individual cultured cortical neurons.

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Energy deficiency and dysfunction of the Na+, K+-ATPase are common consequences of many pathological insults. The nature and mechanism of cell injury induced by impaired Na+, K+-ATPase, however, are not well defined. We used cultured cortical neurons to examine the hypothesis that blocking the Na+,

Ouabain-containing Euro-Collins solution prevents acute tubular necrosis following kidney preservation.

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EVALUATION OF CAFFEINE AND OUABAIN AS PERMISSIVE AGENTS IN THE PRODUCTION OF MYOCARDIAL NECROSIS.

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Ouabain-resistant mechanism of volume control and the ultrastructural organization of liver slices recovering from swelling in vitro.

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We have studied the net extrusion of water by liver slices recovering from swelling at 1 degree C and have attempted to relate this to ultrastructural alterations. Special attention was paid to the ouabain-resistant extrusion of water. The restoration of many details of intracellular architecture

Cochlear function after selective spiral ganglion cells degeneration induced by ouabain.

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BACKGROUND Ouabain, a cardiac glycoside that specifically binds to Na/K-ATPase and inhibits its activity, was applied to gerbils to develop a method for studying auditory neuropathy. METHODS Ouabain was applied to the round window of the cochlea in each gerbil by using a piece of gelfoam with 3

The effect of ouabain on hearts of cardiomyopathic hamsters: potentiation by isoproterenol.

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The isometric twitch properties of papillary muscles from hearts of 30- to 53-day-old cardiomyopathic hamsters (BIO 14.6) were studied before and after exposure to the cardiac glycoside, ouabain. The diseased tissue was weakly responsive to ouabain (3 to 100 microM), as compared to a more

Cardenolide aglycones inhibit tumor necrosis factor α-induced expression of intercellular adhesion molecule-1 at the translation step by blocking Na⁺/K⁺-ATPase.

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Cardiac glycosides, which are inhibitors of Na(+)/K(+)-ATPase, are classified into cardenolides and bufadienolides. We have recently shown that two cardenolide glycosides, ouabain and odoroside A, inhibit Na(+)/K(+)-ATPase, thereby preventing nuclear factor κB-inducible protein expression by

[The role of ouabain in cell death of vascular endothelial cells ECV304 and the changes of expression of Na+, K(+)-ATPase alpha1, beta1-subunit].

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OBJECTIVE To study the effect of Na+, K(+)-ATPase inhibition by ouabain on growth and death of vascular endothelial cells ECV304 and involved mechanisms. METHODS Growth inhibition of ouabain on ECV304 cells was analyzed using MTT assay. The feature of cell death was studied by Hoechst 33342/PI

The neurotoxicity of ouabain, a sodium-potassium ATPase inhibitor, in the rat hippocampus.

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Intrahippocampal injection of 1 nmol ouabain, a sodium/potassium (Na+,K(+)-)ATPase inhibitor, produced a necrotic lesion within 4 days, characterised by a massive invasion by foaming macrophages. A lower dose of ouabain (0.1 nmol) produced a more discrete lesion of all groups of neuronal perikarya

Ouabain-induced perturbations in intracellular ionic homeostasis regulate death receptor-mediated apoptosis.

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Apoptosis is defined by specific morphological and biochemical characteristics including cell shrinkage (termed apoptotic volume decrease), a process that results from the regulation of ion channels and plasma membrane transporter activity. The Na(+)-K(+)-ATPase is the predominant pump that controls

Ouabain-Induced Cell Death and Survival. Role of α1-Na,K-ATPase-Mediated Signaling and [Na ⁺] _i/[K ⁺] _i-Dependent Gene Expression

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Ouabain is of cardiotonic steroids (CTS) family that is plant-derived compounds and is known for many years as therapeutic and cytotoxic agents. They are specific inhibitors of Na,K-ATPase, the enzyme, which pumps Na⁺ and K⁺ across plasma membrane of animal cells. Treatment of

Influence of N-methyl-D-aspartate receptors on ouabain activation of nuclear factor-κB in the rat hippocampus.

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It has been shown that ouabain (OUA) can activate the Na,K-ATPase complex and mediate intracellular signaling in the central nervous system (CNS). Inflammatory stimulus increases glutamatergic transmission, especially at N-methyl-D-aspartate (NMDA) receptors, which are usually coupled to the

Adenine nucleotides, transport activity and hypoxic necrosis in the thick ascending limb of Henle.

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Thick ascending limb of Henle (TAL) necrosis in the isolated perfused kidney is an important model of renal hypoxia, but physiologic and metabolic correlation with this morphologic damage has been inadequate. More precise estimation of TAL adenine nucleotides in this model was obtained in the

Long-term effects of tumor necrosis factor on LLC-PK1 transepithelial resistance.

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Renal epithelial LLC-PK1 cell sheets incubated with tumor necrosis factor (TNF) undergo an acute, spontaneous, and rapidly reversible decrease in transepithelial resistance (TER). (Mullin et al., 1992). However, 24 to 72 h following TNF exposure, TER across the cell sheet increases 2-fold. This

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ouabain/necroză

Na+/K+ pump and endothelial cell survival: [Na+]i/[K+]i-independent necrosis triggered by ouabain, and protection against apoptosis mediated by elevation of [Na+]i.

Ionic mechanism of ouabain-induced concurrent apoptosis and necrosis in individual cultured cortical neurons.

Ouabain-containing Euro-Collins solution prevents acute tubular necrosis following kidney preservation.

EVALUATION OF CAFFEINE AND OUABAIN AS PERMISSIVE AGENTS IN THE PRODUCTION OF MYOCARDIAL NECROSIS.

Ouabain-resistant mechanism of volume control and the ultrastructural organization of liver slices recovering from swelling in vitro.

Cochlear function after selective spiral ganglion cells degeneration induced by ouabain.

The effect of ouabain on hearts of cardiomyopathic hamsters: potentiation by isoproterenol.

Cardenolide aglycones inhibit tumor necrosis factor α-induced expression of intercellular adhesion molecule-1 at the translation step by blocking Na⁺/K⁺-ATPase.

[The role of ouabain in cell death of vascular endothelial cells ECV304 and the changes of expression of Na+, K(+)-ATPase alpha1, beta1-subunit].

The neurotoxicity of ouabain, a sodium-potassium ATPase inhibitor, in the rat hippocampus.

Ouabain-induced perturbations in intracellular ionic homeostasis regulate death receptor-mediated apoptosis.

Ouabain-Induced Cell Death and Survival. Role of α1-Na,K-ATPase-Mediated Signaling and [Na +] i/[K +] i-Dependent Gene Expression

Influence of N-methyl-D-aspartate receptors on ouabain activation of nuclear factor-κB in the rat hippocampus.

Adenine nucleotides, transport activity and hypoxic necrosis in the thick ascending limb of Henle.

Long-term effects of tumor necrosis factor on LLC-PK1 transepithelial resistance.

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Ouabain-Induced Cell Death and Survival. Role of α1-Na,K-ATPase-Mediated Signaling and [Na ⁺] _i/[K ⁺] _i-Dependent Gene Expression