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antidiabetic/hypoxia
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Anti-inflammatory and neuroprotective effects of magnolol in chemical hypoxia in rat cultured cortical cells in hypoglycemic media.
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Our previous studies demonstrated that magnolol protects neurons against chemical hypoxia by KCN in cortical neuron-astrocyte mixed cultures (14). In the present study, we examined whether the neuroprotective effect of magnolol involve modulating inflammatory mediators, prostaglandin E2 (PGE2) and
Antidiabetic sulfonylureas: localization of binding sites in the brain and effects on the hyperpolarization induced by anoxia in hippocampal slices.
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The distribution of antidiabetic sulfonylurea [( 3H]glibenclamide) binding sites is heterogeneous in rat brain. Pyramidal and extrapyramidal motor system contain the highest densities of sites, particularly in the substantia nigra and in the globus pallidus. Only low levels are present in the
Human Adipose-Derived Mesenchymal Stem Cells Respond to Short-Term Hypoxia by Secreting Factors Beneficial for Human Islets In Vitro and Potentiate Antidiabetic Effect In Vivo.
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Adipose-derived mesenchymal stem cells (ASCs) release factors beneficial for islets in vitro and protect against hyperglycemia in rodent models of diabetes. Oxygen tension has been shown to induce metabolic changes and alter ASCs' release of soluble factors. The effects of hypoxia on the
Orexin-A promotes Glu uptake by OX1R/PKCα/ERK1/2/GLT-1 pathway in astrocytes and protects co-cultured astrocytes and neurons against apoptosis in anoxia/hypoglycemic injury in vitro.
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Orexin-A, which is an endogenous neuropeptide, is reported to have a protective role in ischemic stroke. High-concentration glutamic acid (Glu) induced by hypoxia injury in ischemic stroke can be inhibited by glial glutamate transporter GLT-1 which is only expressed in astroglia cells. A previous
The impact of hypoxia on in vivo glucose uptake in a hypoglycemic fish, Myoxocephalus scorpius.
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The mechanisms controlling carbohydrate utilization in teleost fish are poorly understood, particularly in the heart. Tissue glucose uptake and cardiovascular characteristics were measured in the short-horned sculpin, Myoxocephalus scorpius, a species exhibiting low blood glucose levels, during
Depletion of ATP and release of presynaptic inhibition in the CA1 region of hippocampal slices during hypoglycemic hypoxia.
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Transient recovery (TR) of evoked synaptic potentials and ATP depletion during the late stage of hypoxic hypoglycemic insults were investigated in rat hippocampal slices. TR was observed not only in the late stage of insult, but also during recovery. The concentration of ATP corresponded to the
The anti-diabetic drug metformin inhibits vascular endothelial growth factor expression via the mammalian target of rapamycin complex 1/hypoxia-inducible factor-1α signaling pathway in ELT-3 cells.
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The aim of this study was to elucidate whether metformin can regulate the expression of vascular endothelial growth factor (VEGF) in rat-derived uterine leiomyoma cells (ELT-3 cells). In vitro studies were conducted using ELT-3 cells. Under normoxic conditions, metformin suppressed VEGF protein
Uncoupling hypoxia signaling from oxygen sensing in the liver results in hypoketotic hypoglycemic death.
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As the ultimate electron acceptor in oxidative phosphorylation, oxygen plays a critical role in metabolism. When oxygen levels drop, heterodimeric hypoxia-inducible factor (Hif) transcription factors become active and facilitate adaptation to hypoxia. Hif regulation by oxygen requires the protein
Hyperbaric oxygen toxicity in brain: A case of hyperoxia induced hypoglycemic brain syndrome.
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Hyperbaric oxygen exposure is a recent hazzard for higher animals that originated as humans began underwater construction, exploration, and sports. Exposure can lead to abnormal brain EEG, convulsions, and death, the time to onset of each stage of pathology decreasing with increase in oxygen
Hypoxia causes glucose intolerance in humans.
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Hypoxic respiratory diseases are frequently accompanied by glucose intolerance. We examined whether hypoxia is a cause of glucose intolerance in healthy subjects. In a double-blind within-subject crossover design, hypoxic versus normoxic conditions were induced in 14 healthy men for 30 minutes by
Glutathione protects against hypoxic/hypoglycemic decreases in 2-deoxyglucose uptake and presynaptic spikes in hippocampal slices.
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The effects of glutathione, its analogue: YM737 (N-(N-gamma-L-glutamyl-L- cysteinyl) glycine l-isopropyl ester sulfate monohydrate), a monoester of glutathione, and N-acetyl-L-cysteine on hypoxia/hypoglycemia-induced decreases in CA1 presynaptic fiber spikes and 2-deoxyglucose uptake were
NG-nitro-L-arginine protects against hypoxia/hypoglycemia-induced decrease in CA1 presynaptic spikes in rat hippocampal slices.
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The effects of nitric oxide (NO) synthase inhibitors on the hypoxia/hypoglycemia-induced decrease in CA1 presynaptic fiber spikes elicited by stimulation of the Schaffer collaterals were investigated using rat hippocampal slices. Drugs were added to normal medium for 10 min before incubation under
Teneligliptin protects against hypoxia/reoxygenation-induced endothelial cell injury.
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Cardiovascular complications are the main causes of mortality in diabetic patients. Teneligliptin is a newly developed anti-diabetic agent. It has been reported that teneligliptin has a vascular protective capacity in preclinical studies and diabetes patients. In this study, we investigated the
Contributions of Na+ flux and the anoxic depolarization to adenosine 5'-triphosphate levels in hypoxic/hypoglycemic rat hippocampal slices.
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A 10 min exposure of rat hippocampal slices to hypoxic/hypoglycemic medium decreased tissue adenosine 5'-triphosphate (ATP) levels. Hypoxia/hypoglycemia also caused an anoxic depolarization and essentially no recovery of the synaptically evoked population spike from CA1 region recorded 30 min after
Cerebral carbohydrate metabolism during hypoglycemia and anoxia in newborn rats.
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The cerebral metabolic responses to perinatal hypoglycemia and anoxia were studied in newborn rats given regular insulin (30 units per kilogram of body weight). Animals were observed for up to 2 hours with no apparent ill effects in spite of blood glucose concentrations of 0.75 mmol per liter. When
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