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isothiocyanate/hypoxia

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صفحه 1 از جانب 131 نتایج
Two-dimensional fluorescence-based difference gel electrophoresis (DIGE) was used in combination with matrix-assisted laser desorption/ionization tandem time-of-flight mass spectrometry (MALDI-TOF/TOF-MS) to identify a set of hypoxia-related biomarker proteins in medaka (Oryzias latipes) brain

Inhibition of hypoxia inducible factor by phenethyl isothiocyanate.

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Phenethyl isothiocyanate (PEITC), a natural dietary isothiocyanate, has anti-cancer activity in various in vitro and in vivo models. PEITC inhibits angiogenesis but the molecular mechanisms that underlie this effect are not known. We have now demonstrated that PEITC is an effective inhibitor of

Phenethyl isothiocyanate inhibits hypoxia-induced accumulation of HIF-1α and VEGF expression in human glioma cells.

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Phenethyl isothiocyanate (PEITC), a natural dietary isothiocyanate, inhibits angiogenesis but the molecular mechanisms that underlie this effect are not known. In this study, under hypoxic conditions (1% O2), we examined the effect of PEITC on the intracellular level of the hypoxia inducible factor

Role of endoplasmic reticular stress in aortic endothelial apoptosis induced by intermittent/persistent hypoxia.

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BACKGROUND Accumulated evidence shows that hypoxia can induce endothelial apoptosis, however the mechanism is still unknown. We hypothesized whether intermittent or persistent hypoxia could induce endoplasmic reticular stress, leading to endothelial apoptosis. METHODS Twenty-four 8-week male Sprague

The effects of intravenous naltrindole and naltrindole 5'-isothiocyanate on sufentanil-induced respiratory depression and antinociception in rats.

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Although the interactions between the mu- and the delta-opiate receptor subtypes are well documented with regard to supraspinal analgesia, less is known about the mutual interactions on respiratory depression. To clarify the functional interactions between both opiate receptor subtypes with regard

Triamcinolone suppresses retinal vascular pathology via a potent interruption of proinflammatory signal-regulated activation of VEGF during a relative hypoxia.

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We examined the effect of triamcinolone acetonide (TA), a corticosteroid, on the relationship between vascular pathophysiology and vascular endothelial growth factor (VEGF) activation in the retina of a rat model of oxygen-induced retinopathy (OIR). OIR was induced by exposure of hyperoxia (80%

MYBL2 protects against H9c2 injury induced by hypoxia via AKT and NF‑κB pathways.

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Cardiovascular diseases have become one of the major public health problems in many countries. The downregulation of MYBL2 was found in H9c2 and native cardiomyocytes cells after hypoxia treatment. The present study aimed to investigate the effects of MYB proto‑oncogene like 2 (MYBL2) on H9c2 injury

Hypoxemia/reoxygenation down-regulates interleukin-8-stimulated bactericidal activity of polymorphonuclear neutrophil by differential regulation of CD16 and CD35 mRNA expression.

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BACKGROUND The purpose of this study was to determine the effects of hypoxemia/reoxygenation (H/R) on the regulation of interleukin-8 (IL-8)-stimulated human polymorphonuclear neutrophil (PMN) bactericidal activity. METHODS Venous human whole blood was rendered normoxic (Pvo2 saturation 60% to 80%),

Development of hypoxia in a preclinical model of tumor micrometastases.

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OBJECTIVE Hypoxic regions have been shown to be a characteristic feature of a wide variety of human primary tumors, whereas the oxygenation status of subclinical micrometastases is in general unknown. The development of hypoxia in a xenograft model of microscopic metastases was investigated in this

Cytokine control of PMN phagocytosis: regulatory effects of hypoxemia and hypoxemia-reoxygenation.

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We investigated the effects of hypoxemia and hypoxemia-reoxygenation (H/R) on interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), or IL-1beta stimulation of whole blood polymorphonuclear leukocyte (PMN) phagocytosis and bactericidal activity. Whole blood PMN were rendered hypoxemic

Sulforaphane blocks hypoxia-mediated resistance to TRAIL-induced tumor cell death.

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Hypoxia occurs frequently in various solid tumors and elicits a cellular response designed to improve cell survival through adaptive processes, thereby accelerating cancer progression and the development of chemotherapy resistance. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a

Hypoxemia up-regulates interleukin-8 stimulated phagocytosis of polymorphonuclear leukocytes by differential regulation of CD32w and CD35 messenger RNA expression.

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BACKGROUND The purpose of these studies was to investigate the effect of hypoxemia on interleukin-8 (IL-8) regulation of phagocytosis and surface opsonic receptor expression of whole blood polymorphonuclear leukocytes (PMNs). METHODS Whole blood PMNs were rendered hypoxemic (PvO2 less than 15 mm Hg)

Recombinant adeno-associated virus-delivered hypoxia-inducible stanniocalcin-1 expression effectively inhibits hypoxia-induced cell apoptosis in cardiomyocytes.

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Ischemia/hypoxia-induced oxidative stress is detrimental for the survival of cardiomyocytes and cardiac function. Stanniocalcin-1 (STC-1), a glycoprotein, has been found to play an inhibitory role in the production of reactive oxygen species (ROS). Here, we speculated that the overexpression of

The synergistic effects of hypoxia/reoxygenation or tissue acidosis and bacteria on intestinal epithelial cell apoptosis.

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BACKGROUND Clinical data indicate that gut perfusion deficits must be rectified within 24 hours after traumatic injury to decrease organ failure and death. Ischemia/reperfusion injury to the gut causes enterocyte apoptosis (Apo), which may contribute to intestinal barrier failure. The temporal

Neuroprotective effects of Rhizoma Dioscoreae polysaccharides against neuronal apoptosis induced by in vitro hypoxia.

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Rhizoma Dioscoreae polysaccharides (RDPS) are the primary active ingredient of Rhizoma Dioscoreae, which is a traditional Chinese medicine. RDPS have previously been shown to scavenge reactive oxygen species, and protect against D-galactose-induced mimetic aging. The present study aimed to
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