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Página 1 a partir de 196 resultados
Prevention of nerve edema and increased blood-nerve barrier permeability-surface area product in galactosemic rats by aldose reductase or thromboxane synthetase inhibitors.
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Nerve water content and the permeability-surface area product (PA) to [3H]-or [14C]sucrose at the blood-nerve barrier were determined in unanesthetized control rats fed a normal diet and in rats fed galactose with or without an aldose reductase inhibitor (Statil or AL 1576) or a thromboxane
Edema and increased endoneurial sodium in galactose neuropathy. Reversal with an aldose reductase inhibitor.
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Galactose neuropathy was produced in rats by feeding a diet containing 30% D-galactose. After 12 weeks of galactose ingestion, all rats developed bilateral cataracts, polydypsia and polyuria. These galactose-intoxicated animals were divided into two groups that both continued with the galactose
Tat-biliverdin reductase A inhibits inflammatory response by regulation of MAPK and NF-κB pathways in Raw 264.7 cells and edema mouse model.
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Reactive oxygen species (ROS) accumulation induces oxidative stress and cell damage, which then activates several signaling pathways and triggers inflammatory response. Biliverdin is a natural product of heme metabolism which is converted to bilirubin by the enzyme biliverdin reductase A (BLVRA)
Benzo(a)pyrene-induced pulmonary inflammation, edema, surfactant dysfunction, and injuries in rats: alleviation by farnesol.
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Benzo(a)pyrene (B(a)P) is a well-known environmental contaminant and carcinogen. Its sources include tobacco smoke, automobile exhaust, forest fire, and other combustion processes. Farnesol, an active principle of Vachellia farnesiana and other aromatic plants, possesses preventive properties
Stimulation of astrocytes affects cytotoxic brain edema.
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Cytotoxic brain edema has been produced in rats by subacute intoxication with triethyltin (TET). Some animals were allowed to recover spontaneously, others were post-treated with an extract of Ginkgo biloba (EGB) for 1 to 4 weeks, beginning 3 days after intoxication was stopped. The time course of
Attenuating brain edema, hippocampal oxidative stress, and cognitive dysfunction in rats using hyperbaric oxygen preconditioning during simulated high-altitude exposure.
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BACKGROUND
We assessed whether hyperbaric oxygen preconditioning (HBO2P) in rats induced heat shock protein (HSP)-70 and whether HSP-70 antibody (Ab) preconditioning attenuates high altitude exposure (HAE)-induced brain edema, hippocampal oxidative stress, and cognitive dysfunction.
METHODS
Rats
[The effects of taurine on oxidative processes in brain edema].
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OBJECTIVE
To investigate the free radical oxidation of lipids, oxidative modification of protein activity of glutathione peroxidase and glutathione reductase as well as the end product of nitric oxide - nitrite in the brain mitochondrial fraction of animals with experimentally induced cerebral edema
Diabetic macular edema: classification, medical and laser therapy.
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OBJECTIVE
to propose and describe a new classification of diabetic macular edema (DME) based on its etiopathogenetic features and to present efficacy and safety data on medical and laser treatments currently used and under investigation.
METHODS
available literature on DME has been reviewed and
Methylenetetrahydrofolate reductase gene polymorphism and glucocorticoid intake in children with ALL and aseptic osteonecrosis.
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BACKGROUND
Methotrexate is an essential part of the treatment of acute lymphoblastic leukaemia (ALL). Due to an increased survival of ALL patients, complications like BME (bone marrow edema) and AON (aseptic osteonecrosis) have become a matter of increasing importance. The aim of the study was to
Prior use of 3-hydroxy-3-methyl-glutaryl-coenzyme a reductase inhibitor, simvastatin fails to improve outcome after experimental intracerebral hemorrhage.
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OBJECTIVE
Contrary to some clinical belief, there were quite a few studies regarding animal models of intracerebral hemorrhage (ICH) in vivo suggesting that prior use of statins may improve outcome after ICH. This study reports the effect of 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG CoA) reductase
Activities of lung NADPH-cytochrome C-reductase and of cytochrome P-450 peroxidase during the protection of rat from hyperoxic injury by polyriboinosinic acid-polyribocytidilic acid.
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Rats exposed to normobaric oxygen received a single i.p. injection of 2.5 mg/kg of poly I: poly C at various times (-120 to +36 h) before and after the beginning of oxygen exposure. Hyperoxic lung damage and modifications in cytochrome P-450 system components were evaluated. Our results confirmed
Localization of aldose reductase and sorbitol dehydrogenase in the nervous system of normal and diabetic rats.
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Intraneuronal accumulations of sorbitol and fructose have been postulated to predispose the nervous system to the cerebral edema associated with the treatment of diabetic ketoacidosis. In the present study, the enzymes of the pathway for the production of sorbitol and fructose, aldose reductase and
Gene deletion and pharmacological inhibition of aldose reductase protect against retinal ischemic injury.
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Retinal ischemic injury is common in patients with diabetes, atherosclerosis, hypertension, transient ischemia attack and amaurosis fugax. Previously, signs of ischemic stress, such as pericyte loss, blood-retinal barrier breakdown and neovascularization, which can lead to occlusion of retinal
Smith-Lemli-Opitz syndrome presenting with persisting nuchal oedema and non-immune hydrops.
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Smith-Lemli-Opitz syndrome (SLO) is a recognized clinical entity with distinctive anomalies. Recently it has been shown that a specific defect in cholesterol metabolism, 7-dehydroxycholesterol reductase deficiency, causes the multiple abnormalities seen in SLO. There have been two reports of
Effects of an aldose reductase inhibitor, SNK-860, on the histopathological changes of retinal tissues in a streptozotocin-induced diabetic rat model.
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In order to clarify the mechanism of retinal tissue damage in diabetes mellitus, the effects of the inhibition of aldose reductase on the pathologic changes in the retina of streptozotocin-induced diabetic (STZ-diabetic) rats were examined histologically and histochemically. The STZ-diabetic animals
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