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Sida 1 från 19 resultat
Differential activation pattern of redox-sensitive transcription factors and stress-inducible dilator systems heme oxygenase-1 and inducible nitric oxide synthase in hemorrhagic and endotoxic shock.
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OBJECTIVE
To investigate the role of redox-sensitive transcription factors nuclear factor kappa-B (NF-kappaB) or activator protein-1 (AP-1) for hepatic gene expression of heme oxygenase (HO)-1 and inducible nitric oxide synthase (iNOS) in models of hemorrhagic or endotoxic shock.
METHODS
Prospective
Role of Oxidative Stress on Vaginal Bleeding during The First Trimester of Pregnant Women.
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BACKGROUND
Reactive oxygen species (ROS) are produced in many metabolic and physiologic processes. Antioxidative mechanisms remove these harmful species. Our aim was to assess whether serum total antioxidant capacity and total oxidant status altered during first trimester pregnancies with vaginal
Hepatic redox regulation of transcription factors activator protein-1 and nuclear factor-kappaB after hemorrhagic shock in vivo.
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Ischemia and reperfusion result in a hepatocellular stress gene response, characterized by a zonal heterogeneity with pericentral hepatocytes being the primary target. In the present study, we assessed cell type-specific and zonal pattern of activation of redox-sensitive transcription factors
Trans-sodium crocetinate and hemorrhagic shock.
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Trans-sodium crocetinate (TSC) has been found to alleviate the symptoms of hemorrhagic shock in that, after the drug is given to hemorrhaged rats, blood pressure rises, elevated lactate levels are reduced, cellular damage in the liver and kidney is less, and survival is increased. The mechanism of
Kupffer cell inactivation by carbon monoxide bound to red blood cells preserves hepatic cytochrome P450 via anti-oxidant and anti-inflammatory effects exerted through the HMGB1/TLR-4 pathway during resuscitation from hemorrhagic shock.
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Red blood cell (RBC) transfusions for controlling hemorrhaging induce systemic ischemia reperfusion, resulting in a decrease in hepatic cytochrome P450 (CYP) levels. Carbon monoxide (CO), when bound to red blood cells (CO-RBC) has the potential to protect the hepatic CYP protein to produce a
Differential expression pattern of heme oxygenase-1/heat shock protein 32 and nitric oxide synthase-II and their impact on liver injury in a rat model of hemorrhage and resuscitation.
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OBJECTIVE
To investigate the role of the vasodilator systems heme oxygenase-1/heat shock protein 32 (HO-1/HSP32) and nitric oxide synthase-II (NOS-II), generating carbon monoxide and nitric oxide respectively, as modulators of liver injury in an experimental model of reversible hemorrhagic
Role of reactive oxygen species for hepatocellular injury and heme oxygenase-1 gene expression after hemorrhage and resuscitation.
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Reactive oxygen species (ROS) generated during hemorrhage and subsequent resuscitation (H/R) may contribute to cellular injury but may also regulate an adaptive cellular response to stress. Heme oxygenase (HO)-1 has been recognized as an important stress-inducible gene conferring protection after
Neurotoxicity of hemoglobin in cortical cell culture.
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Hemoglobin (Hb) has been demonstrated to be neurotoxic when injected into the cerebral cortex in vivo. However, associated systemic factors such as ischemia and epileptogenesis have limited investigations of Hb toxicity in the intact central nervous system (CNS). In this study, the neurotoxicity of
Anti-oxidant treatment for shock: vitamin E but not vitamin C improves survival.
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Anti-oxidant therapy has been effective for treatment of experimental shock. In this study, the efficacy of Trolox (Aldrich Chemical Co., Milwaukee, WI), a water-soluble vitamin E analogue, and ascorbic acid (vitamin C) was evaluated in a rat model of hemorrhagic shock and resuscitation. In two
Melatonin prevents focal rat cerebellum injury as assessed by induction of heat shock protein (HO-1) following subarachnoid injections of lysed blood.
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The present paper studies a marker of oxidative stress such as heme oxygenase-1 (HO-1), the main heat shock protein. HO-1 expression was induced in the focal region of the cerebellum following experimental subarachnoid hemorrhage (SAH). Lysed blood was injected into the subarachnoid space or
Thiamine Deficiency Modulates p38MAPK and Heme Oxygenase-1 in Mouse Brain: Association with Early Tissue and Behavioral Changes.
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Thiamine deficiency (TD) produces severe neurodegenerative lesions. Studies have suggested that primary neurodegenerative events are associated with both oxidative stress and inflammation. Very little is known about the downstream effects on intracellular signaling pathways involved in neuronal
Iron accumulation and neurotoxicity in cortical cultures treated with holotransferrin.
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Nonheme iron accumulates in CNS tissue after ischemic and hemorrhagic insults and may contribute to cell loss. The source of this iron has not been precisely defined. After blood-brain barrier disruption, CNS cells may be exposed to plasma concentrations of transferrin-bound iron (TBI), which exceed
Pretreatment of human amnion-chorion with vitamins C and E prevents hypochlorous acid-induced damage.
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OBJECTIVE
Preterm premature rupture of fetal membranes has been associated with infection, cigarette smoking, and bleeding. Hypochlorous acid (a reactive oxygen species) is central to the body's response to infection, yet it may damage surrounding tissue while destroying pathogens. We examined in
Inhibition of amyloid-beta-induced cell death in human brain pericytes in vitro.
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Amyloid-beta protein (A beta) deposition in the cerebral vascular walls is one of the key features of Alzheimer's disease and hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D). A beta(1-40) carrying the 'Dutch' mutation (HCHWA-D A beta(1-40)) induces pronounced degeneration of
The metabolism and toxicity of hemin in astrocytes.
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Hemin is cytotoxic, and contributes to the brain damage that accompanies hemorrhagic stroke. In order to better understand the basis of hemin toxicity in astrocytes, the present study quantified hemin metabolism and compared it to the pattern of cell death. Heme oxygenase-1 (HO-1) expression was
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