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Страница 1 от 139 полученные результаты
Trolox and 6,7-dinitroquinoxaline-2,3-dione prevent necrosis but not apoptosis in cultured neurons subjected to oxygen deprivation.
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There is a growing body of evidence suggesting that apoptosis is involved in ischemic brain injury. Recent studies suggest that a rapid necrosis masked a more subtle apoptotic death in neurons subjected to oxygen deprivation in culture. To test this hypothesis, we treated cultured neurons with
Ceramide-induced formation of ROS and ATP depletion trigger necrosis in lymphoid cells.
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In lymphocytes, Fas activation leads to both apoptosis and necrosis, whereby the latter form of cell death is linked to delayed production of endogenous ceramide and is mimicked by exogenous administration of long- and short-chain ceramides. Here molecular events associated with noncanonical
Nerve growth factor potentiates the oxidative necrosis of striatal cholinergic neurons.
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We examined the effects of nerve growth factor (NGF) on free radical neurotoxicity in striatal cell cultures. Following exposure to 30 microM Fe2+ or 1 mM L-buthionine-[S,R]-sulfoximine (BSO), an inhibitor of gamma-glutamylcysteine synthetase, striatal neurons underwent cell body swelling and then
Glutamate neurotoxicity in mouse cortical neurons: atypical necrosis with DNA ladders and chromatin condensation.
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The possibility that glutamate may induce neuronal apoptosis was examined in cultured cortical neurons. Neurons underwent widespread death 24 h following exposure to 50 microM glutamate. The glutamate neurotoxicity was blocked by inclusion of the glutamate antagonists, 10 microM MK-801 and 50 microM
NT-4/5 exacerbates free radical-induced neuronal necrosis in vitro and in vivo.
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Neurotrophins render neurons highly vulnerable to certain injuries. We examined the possibility that NT-4/5 would enhance free radical neurotoxicity in vivo as well as in vitro. Striatal neurons exposed to 10 microM Fe(2+) or 1 mM l-buthionine-[S, R]-sulfoximine (BSO) underwent mild degeneration
Removal of glutathione produces apoptosis and necrosis in HepG2 cells overexpressing CYP2E1.
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BACKGROUND
Previous studies have shown that addition of ethanol, iron, or arachidonic acid to HepG2 cells expressing CYP2E1 produced a loss in cell viability and caused apoptosis. These effects were enhanced when cellular reduced glutathione (GSH) levels were lowered by treatment with buthionine
Liver glutathione depletion induced by bromobenzene, iodobenzene, and diethylmaleate poisoning and its relation to lipid peroxidation and necrosis.
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The mechanisms of bromobenzene and iodobenzene hepatotoxicity in vivo were studied in mice. Both the intoxications caused a progressive decrease in hepatic glutathione content. In both instances liver necrosis was evident only when the hepatic glutathione depletion reached a threshold value (3.5-2.5
Trimethyltin-activated cyclooxygenase stimulates tumor necrosis factor-alpha release from glial cells through reactive oxygen species.
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Exposure of a primary culture of glial cells to the classical neurotoxicant trimethyltin (TMT) results in the release of prostaglandin (PG)E(2) and tumor necrosis factor (TNF)-alpha. Prior treatment of glial cells with either the nonspecific inhibitor of cyclooxygenase and lypoxygenase
Attenuation of oxidative neuronal necrosis by a dopamine D1 agonist in mouse cortical cell cultures.
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Events which lead to an increase in intracellular free radicals induce necrotic cell death of cultured cortical neurons. In the present study, we report that treatment with 1 microM (+/-)-SKF-38393 hydrochloride, a selective D1 agonist, as well as 100 microM trolox, a lipophilic vitamin E analogue,
Trolox down-regulates transforming growth factor-beta and prevents experimental cirrhosis.
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Cirrhosis is a very common disease and its treatment is limited due to lack of effective drugs. Some studies indicate that this disease is associated with oxidative stress. Therefore, we decided to study the effect of trolox, an effective antioxidant, on experimental cirrhosis. Cirrhosis was induced
The effects of Trolox, a water-soluble vitamin E analogue, in regionally ischemic, reperfused porcine hearts.
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Myocardial protection by the water-soluble vitamin E analogue, Trolox, was investigated in 18 regionally ischemic, reperfused porcine hearts. The left anterior descending coronary artery was distally ligated for 45 min and was reperfused for three days. Five grams of Trolox (n = 9) were infused
Reduction of experimental myocardial infarct size by infusion of lactosylphenyl Trolox.
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OBJECTIVE
The aim was to determine if lactosylphenyl Trolox could improve myocardial resistance to ischaemia and reperfusion. Lactosylphenyl Trolox is derived by coupling p-aminophenyl-beta-D-lactopyranoside to Trolox. Trolox, a polar analogue of vitamin E, has been found to protect human
Protective effect of photodegradation product of nifedipine against tumor necrosis factor alpha-induced oxidative stress in human glomerular endothelial cells.
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Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nitrosonifedipine (NO-NIF) is metabolically and photochemically produced from nifedipine, and NO-NIF
Effect of Trolox on altered vasoregulatory gene expression in hepatic ischemia/reperfusion.
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This study was designed to investigate the effect of Trolox, a hydrophilic analogue of vitamin E, on the alteration of vasoregulatory gene expression during hepatic ischemia and reperfusion (I/R). Rats were subjected to 60 min of hepatic ischemia in vivo. The rats were treated intravenously with
Purpurogallin is a more powerful protector of kidney cells than Trolox and allopurinol.
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Phase contrast and electron microscopic experiments demonstrated that oxyradicals generated with xanthine oxidase and hypoxanthine markedly damage rat kidney mesangial and porcine tubular epithelial cells. Purpurogallin, a phenol found in oak nutgalls, prolongs survival of the xanthine oxidase
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