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pyrrolidine/hypoxia
Veza se sprema u međuspremnik
Stranica 1 iz 76 rezultatima
Antioxidant pyrrolidine dithiocarbamate activates Akt-GSK signaling and is neuroprotective in neonatal hypoxia-ischemia.
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Pyrrolidine dithiocarbamate (PDTC), an antioxidant and inhibitor of transcription factor nuclear factor kappa-B (NF-kappaB), has been reported to reduce inflammation and apoptosis. Because PDTC was recently found to protect in various models of adult brain ischemia with a wide therapeutic time
Intranasal pyrrolidine dithiocarbamate decreases brain inflammatory mediators and provides neuroprotection after brain hypoxia-ischemia in neonatal rats.
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Brain injury due to birth asphyxia is the major cause of death and long-term disabilities in newborns. We determined whether intranasal pyrrolidine dithiocarbamate (PDTC) could provide neuroprotection in neonatal rats after brain hypoxia-ischemia (HI). Seven-day old male and female Sprague-Dawley
Inhibition of NF kappa B activation by pyrrolidine dithiocarbamate prevents in vivo hypoxia/reoxygenation-mediated myocardial angiogenesis.
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This study sought to examine the effect of nonlethal moderate whole body hypoxic challenge (10% 02/90% N2) on rat myocardial angiogenesis. Sprague Dawley rats were subjected to 4 h of systemic normobaric hypoxemic hypoxia (10 +/- 0.4% O2) in an anesthesia chamber or to 4 h of normoxia (ambient 20.9
Hypoglycemia induces general neuronal death, whereas hypoxia and glutamate transport blockade lead to selective retinal ganglion cell death in vitro.
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OBJECTIVE
To examine the impact of experimental ischemia and interruption of glutamate transport on retinal neuronal cell, especially retinal ganglion cell (RGC), survival in vitro.
METHODS
Cell cultures were prepared from adult pig retinas and maintained under different experimental conditions of
hCLOCK induction by hypoxia promotes inflammatory responses by activating the NF‑κB pathway.
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The expression and secretion of infla-mmation‑associated cytokines are induced by hypoxia. Circadian locomotor output cycles protein kaput (CLOCK) has previously been shown to activate the nuclear factor‑κB (NF‑κB) pathway, which is a key transcription factor during hypoxia. The present study
Protective effect of L-trans-pyrrolidine-2,4-dicarboxilic acid preload against cell death induced by oxygen/glucose deprivation in differentiated PC12 cells.
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It has been postulated that cellular glutamate is released into the extracellular fluid when the energy supply of the brain is compromised (i.e., anoxia or oxygen/glucose deprivation), and there the amino acid triggers the so-called excitotoxic cascade, causing neuronal death. Several mechanisms for
Hypoxia-induced collagen synthesis of human lung fibroblasts by activating the angiotensin system.
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The exact molecular mechanism that mediates hypoxia-induced pulmonary fibrosis needs to be further clarified. The aim of this study was to explore the effect and underlying mechanism of angiotensin II (Ang II) on collagen synthesis in hypoxic human lung fibroblast (HLF) cells. The HLF-1 cell line
Novel injury mechanism in anoxia and trauma of spinal cord white matter: glutamate release via reverse Na+-dependent glutamate transport.
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Spinal cord injury is a devastating condition, with much of the clinical disability resulting from disruption of white matter tracts. Recent reports suggest a component of glutamate excitotoxicity in spinal cord injury. In this study, the role of glutamate and mechanism of release of this
The migration of neural progenitor cell mediated by SDF-1 is NF-κB/HIF-1α dependent upon hypoxia.
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OBJECTIVE
Stromal cell-derived factor 1 (SDF-1) is critical for neural progenitor cell (NPC) migration after ischemia for nerve repair, but how hypoxic induction of SDF-1 is regulated has not been fully addressed. Here, we examined the regulation of SDF-1 hypoxic induction by the transcription
Effect of nuclear factor-kappa B on vascular endothelial growth factor mRNA expression of human pulmonary artery smooth muscle cells in hypoxia.
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In order to investigate the effect of nuclear factor-kappa B (NF-kappaB) on vascular endothelial growth factor (VEGF) mRNA expression of human pulmonary artery smooth muscle cells (HPASMCs) in hypoxia, the cultured HPASMCs in vitro were stimulated with pyrrolidine dithiocarbamate (PDTC), an
mTOR/NF-κB signaling pathway protects hippocampal neurons from injury induced by intermittent hypoxia in rats.
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Objective: To expound the roles of mTOR and NF-kB signaling pathway in intermittent hypoxia (IH)-induced damage of hippocampal neurons.Methods: For rat experiments, mTOR inhibitor (Rapamycin, Rapa) and NF-κB signaling inhibitor (ammonium pyrrolidine dithiocarbamate, PDTC) were applied
Bis(dialkyl)dithiocarbamato cobalt(III) complexes of bidentate nitrogen mustards: synthesis, reduction chemistry and biological evaluation as hypoxia-selective cytotoxins.
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Cobalt(III) complexes [Co(R2dtc)2(L)]+ containing two dithiocarbamate ligands (R = Me, Et, pyrrolidine) and a bidentate nitrogen mustard ligand (L) have been prepared as potential hypoxia-selective cytotoxins. The complexes were synthesized by treatment of the binuclear precursor [Co2(R2dtc)5]+ with
Hypoxia-induced endothelial apoptosis through nuclear factor-kappaB (NF-kappaB)-mediated bcl-2 suppression: in vivo evidence of the importance of NF-kappaB in endothelial cell regulation.
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The transcription factor nuclear factor-kappaB (NF-kappaB) plays a pivotal role in the coordinated transactivation of cytokine and adhesion molecule genes involved in endothelial activation. Although recent reports have documented the contribution of NF-kappaB to apoptosis, it is still
[Effects of hypoxia on the phenotype transformation of human dermal fibroblasts to myofibroblasts and the mechanism].
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Objective: To investigate the effects of hypoxia on the phenotype transformation of human dermal fibroblasts to myofibroblasts and the mechanism. Methods: The third passage of healthy adult human dermal fibroblasts in logarithmic phase were cultured in DMEM medium containing 10% fetal bovine serum
[Pharmacodynamic bioequivalence of piracetam in hypoxic hypoxia].
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An open cross-over study was run in 8 healthy, younger male volunteers (2 trial days, 7-day wash-out period). After assessment of room air and hypoxia prevalues (10.5% oxygen, inspiratory), 1600 mg 2-oxo-pyrrolidine-1-acetamide (piracetam)--using two commercial formulations (Encetrop and reference
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