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nordihydroguaiaretic acid/hypoxia
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Sivu 1 alkaen 29 tuloksia
Effect of nordihydroguaiaretic acid on cerebral blood flow and metabolism during hypoxia in newborn piglets.
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Nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, was investigated for its effect on cerebral blood flow (CBF) and cortical oxygen consumption during hypoxia in 9 anesthetized, ventilated newborn piglets. CBF was measured by radioactive microspheres while brain cortical metabolism was
NFATc3 pathway participates in the process that 15-LO/15-HETE protects pulmonary artery smooth muscle cells against apoptosis during hypoxia.
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Hypoxia activates nuclear factor of activated T cells isoforms c3 (NFATc3), a Ca(2+)-dependent transcription factor in murine pulmonary arteries (PAs), and NFATc3 has been proved to be implicated in hypoxia-induced pulmonary arterial smooth muscle cells (PASMCs) proliferation, but it remains unclear
Hypoxia provokes leukotriene-dependent neutrophil sequestration in perfused rabbit hearts.
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Isolated rabbit hearts were perfused with salt solution containing autologous 111In-labeled neutrophils to determine whether 1) hypoxia provoked myocardial neutrophil sequestration, 2) neutrophil accumulation could be suppressed by inhibition of lipoxygenase and 3) hypoxic myocardium generated
Effect of arachidonic acid metabolic inhibitors on hypoxia/reoxygenation-induced renal cell injury.
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The present study was undertaken to examine the role of arachidonic acid (AA) metabolites in hypoxia/reoxygenation (H/R)-induced renal cell injury in rabbit renal cortical slices using AA metabolic inhibitors. Inhibitors of cyclooxygenase (indomethacin and diclofenac sodium) and lipoxygenase
Nordihydroguaiaretic acid attenuates NMDA neurotoxicity--action beyond the receptor.
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There is widespread interest in the neurotoxicity of the endogenous excitatory amino acid neurotransmitter glutamate. Excessive glutamate release or accumulation leads to neuronal injury or death in a variety of experimental models of ischemia, anoxia and hypoglycemia. This injury appears to be
Chronic hypoxia enhances 15-lipoxygenase-mediated vasorelaxation in rabbit arteries.
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15-Lipoxygenase (15-LO-1) metabolizes arachidonic acid (AA) to 11,12,15-trihydroxyeicosatrienoic acids (THETAs) and 15-hydroxy-11,12-epoxyeicosatrienoic acids (HEETA) that dilate rabbit arteries. Increased endothelial 15-LO-1 expression enhances arterial relaxations to agonists. We tested the effect
Role of lipoxygenase, cyclooxygenase and cytochrome P-450 metabolites in contractions of isolated guinea pig pulmonary venules induced by hypoxia and anoxia.
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Arachidonic acid metabolites, notably leukotrienes (LTs), have been postulated to play a role in hypoxic pulmonary vasoconstriction. In the present study, we examined the contribution of arachidonic acid metabolites, via the cyclooxygenase, 5-lipoxygenase and cytochrome P-450 monooxygenase pathways,
Nordihydroguaiaretic acid reduces secondary organ injury in septic rats after cecal ligation and puncture
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Background: Nordihydroguaiaretic acid (NDGA) is a plant extract that has been shown to act as a free radical scavenger and pluripotent inhibitor of pro-inflammatory cytokines, two major cellular processes involved in the pathophysiology
mTORC1 is a target of nordihydroguaiaretic acid to prevent breast tumor growth in vitro and in vivo.
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Nordihydroguaiaretic acid (NDGA) is a natural phenolic compound isolated from the creosote bush Larrea divaricata, which has anti-tumor activities both in vitro and in vivo. Its analogs are in clinical development for use in refractory solid tumors. But the mechanisms underlying the anti-cancer
Activation of the Ste20-like oxidant stress response kinase-1 during the initial stages of chemical anoxia-induced necrotic cell death. Requirement for dual inputs of oxidant stress and increased cytosolic [Ca2+].
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Signal transduction mechanisms activated during the early stages of necrotic cell death are poorly characterized. We have recently identified the Sterile 20 (Ste20)-like oxidant stress response kinase-1, SOK-1, which is a member of the Ste20 kinase family. We report that SOK-1 is markedly activated
ROCK pathway participates in the processes that 15-hydroxyeicosatetraenoic acid (15-HETE) mediated the pulmonary vascular remodeling induced by hypoxia in rat.
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15-Hydroxyeicosatetraenoic acid (15-HETE), a product of arachidonic acid (AA) catalyzed by 15-lipoxygenase (15-LO), plays an essential role in hypoxic pulmonary arterial hypertension. We have previously shown that 15-HETE inhibits apoptosis in pulmonary artery smooth muscle cells (PASMCs). To test
Augmentation of hypoxic pulmonary vasoconstriction in the isolated perfused rat lung by in vitro antagonists of endothelium-dependent relaxation.
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The role of the endothelium in hypoxic constriction of the intact pulmonary vascular bed has not been clearly elucidated. To test for a possible role for endothelium-derived relaxing factor(s) (EDRF) in the hypoxic pressor response, isolated, whole blood-perfused rat lungs from male Sprague-Dawley
15-Lipoxygenase and 15-hydroxyeicosatetraenoic acid regulate intravascular thrombosis in pulmonary hypertension.
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Pulmonary arterial hypertension (PAH) is a disease characterized by thickening of pulmonary artery walls, elevated pulmonary vascular resistance, pulmonary vascular thrombotic lesions, and right heart failure. Recent studies suggest that 15-lipoxygenase (15-LO)/15-hydroxyeicosatetraenoic acid
Cardiovascular effects of leukotrienes in neonatal piglets. Role in hypoxic pulmonary vasoconstriction?
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We investigated the effects of exogenous leukotriene D4, synthesis inhibitors, and a leukotriene receptor antagonist upon chloralose anesthetized, mechanically ventilated, neonatal piglets with constant left pulmonary blood flow and upon piglets with uncontrolled pulmonary blood flow. Leukotriene D4
Delayed thromboxane or tumor necrosis factor-alpha, but not leukotriene inhibition, attenuates prolonged pulmonary hypertension in endotoxemia.
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The early phase of endotoxin-induced acute hemodynamic disturbances and hypoxemia is mediated by various factors, including eicosanoids and tumor necrosis factor-alpha (TNF alpha). Thromboxane A2 is the major mediator of the early pulmonary hypertension associated with endotoxemia, but the
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