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2 3 dihydroxybenzoic acid/hypoxia
L'enllaç es desa al porta-retalls
Pàgina 1 des de 27 resultats
Production of hydroxyl radical in the hippocampus after CO hypoxia or hypoxic hypoxia in the rat.
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Carbon monoxide poisoning produces both immediate and delayed neuronal injury in selective regions of the brain that is not readily explained on the basis of tissue hypoxia. One possibility is that cellular injury during and after CO poisoning is related to the production of reactive oxygen species
Hypobaric hypoxia preconditioning attenuates acute lung injury during high-altitude exposure in rats via up-regulating heat-shock protein 70.
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HHP (hypobaric hypoxia preconditioning) induces the overexpression of HSP70 (heat-shock protein 70), as well as tolerance to cerebral ischaemia. In the present study, we hypothesized that HHP would protect against HAE (high-altitude exposure)-induced acute lung injury and oedema via promoting the
Hypoxia-inducible factor stabilizers and other small-molecule erythropoiesis-stimulating agents in current and preventive doping analysis.
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Increasing the blood's capacity for oxygen transport by erythropoiesis-stimulating agents (ESAs) constitutes a prohibited procedure of performance enhancement according to the World Anti-Doping Agency (WADA). The advent of orally bio-available small-molecule ESAs such as hypoxia-inducible factor
Protection of bradykinin on neonatal rat myocytes subjected to anoxia/reoxygenation injury.
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This study was to investigate the effects of bradykinin (BK) on myocyte cultures. The effects of BK against lipid peroxidation and oxygen free radicals were estimated on an anoxia/reoxygenation injured model. A salicylate hydroxylation product dihydroxybenzoic acids (DHBA) was detected using HPLC
Attenuating systemic inflammatory markers in simulated high-altitude exposure by heat shock protein 70-mediated hypobaric hypoxia preconditioning in rats.
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OBJECTIVE
The primary goal of this study was to test whether high-altitude exposure (HAE: 0.9% O(2) at 0.47 ATA for 24 hours) was capable of increasing the systemic inflammatory markers as well as the toxic organ injury indicators in rats, with a secondary goal to test whether preinduction of heat
Hydroxyl radical production in the substantia nigra after 6-hydroxydopamine and hypoxia-reoxygenation.
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To study the involvement of oxidative stress in 6-OHDA neurotoxicity, we investigated the production of the hydroxyl free radical (OH.) in the substantia nigra (SN) and the striatum (CS) several moments after intranigral injection of the neurotoxin, with or without an added episode of hypoxia (30
Prolyl hydroxylase inhibitors depend on extracellular glucose and hypoxia-inducible factor (HIF)-2alpha to inhibit cell death caused by nerve growth factor (NGF) deprivation: evidence that HIF-2alpha has a role in NGF-promoted survival of sympathetic neurons.
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Neurotrophins are critical for the survival of neurons during development and insufficient access to neurotrophins later in life may contribute to the loss of neurons in neurodegenerative disease, spinal cord injury, and stroke. The prolyl hydroxylase inhibitors ethyl 3,4-dihydroxybenzoic acid (DHB)
Effect of melatonin on production of hydroxyl radical and lactate dehydrogenase during hypoxia in rat cortical slices.
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OBJECTIVE
To study the effect of melatonin on the production of hydroxyl radical (.OH) and lactate dehydrogenase (LDH) following hypoxia in cortical slice.
METHODS
Cortical slice was incubated with artificial cerebrospinal fluid (ACSF) in tube. Hypoxia was achieved by substituting 91.6% N2 and 8.4%
Anoxia/reoxygenation induces hydroxyl free radical formation in brain microvessels.
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Isolated rat brain microvessels have been utilized to examine whether they produce hydroxyl free radicals if they are subjected to a 10- to 20-min anoxia period followed by a 40-min reoxygenation period. Hydroxyl free radical flux was assessed utilizing salicylate as a trap. The 2,3- and
Hypoxia response in asthma: differential modulation on inflammation and epithelial injury.
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Oxygen-sensing prolyl-hydroxylase (PHD)-2 negatively regulates hypoxia-inducible factor (HIF)1-α and suppresses the hypoxic response. Hypoxia signaling is thought to be proinflammatory but also attenuates cellular injury and apoptosis. Although increased hypoxic response has been noted in asthma,
Suppression of reactive oxygen species production enhances neuronal survival in vitro and in vivo in the anoxia-tolerant turtle Trachemys scripta.
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Hypoxia-ischemia with reperfusion is known to cause reactive oxygen species-related damage in mammalian systems, yet, the anoxia tolerant freshwater turtle is able to survive repeated bouts of anoxia/reoxygenation without apparent damage. Although the physiology of anoxia tolerance has been much
Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain.
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To better understand the mechanisms of tissue injury during and after carbon monoxide (CO) hypoxia, we studied the generation of partially reduced oxygen species (PROS) in the brains of rats subjected to 1% CO for 30 min, and then reoxygenated on air for 0-180 min. By determining H2O2-dependent
Hydroxyl radical production in the brain after CO hypoxia in rats.
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Reactive oxygen species (ROS) have been implicated in the pathogenesis of neuronal injury after carbon monoxide (CO) poisoning. Severe CO poisoning is treated with hyperbaric oxygen (HBO), which eliminates CO quickly from hemoglobin and body tissue stores, but has a potential to increase ROS
Selective brain hypothermia protects against hypoxic-ischemic injury in newborn rats by reducing hydroxyl radical production.
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We hypothesized that selective brain hypothermia (SBHT) decreases production of hydroxyl radicals (*OH) induced by hypoxia-ischemia (H-I) and reperfusion and attenuates neuronal damage in neonatal rat brain. Anesthetized 7-day-old rats were divided into a normothermia (NT) group (n=6) and a SBHT
Hydroxyl radical generation following ischaemia-reperfusion in cell-free perfused rat kidney.
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The difficulty in direct detection of oxygen-derived free radicals (OFR) in the intact kidney has left uncertain the role of OFR in renal hypoperfusion injury. Salicylate hydroxylation was used as a sensitive method of estimating the extent of production of highly reactive hydroxyl radicals in renal
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