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Страница 1 от 79 резултата
Cellular redistribution of inducible Hsp70 protein in the human and rabbit heart in response to the stress of chronic hypoxia: role of protein kinases,.
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Many infants who undergo cardiac surgery have a congenital cyanotic defect where the heart is chronically perfused with hypoxemic blood. Infant hearts adapt to chronic hypoxemia by activation of intracellular protein kinase signal transduction pathways. However, the involvement of heat shock protein
Baicalein protects chicken embryonic cardiomyocyte against hypoxia-reoxygenation injury via mu- and delta- but not kappa-opioid receptor signaling.
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Baicalein, a pure compound derived from Scutellaria baicalensis Georgi, protected cells from lethal damage in an ischemia-reperfusion model. This study was aimed to investigate the role of opioid receptors in mediating cardioprotection by baicalein against hypoxia-reoxygenation injury. By using
Activation of PKC modulates blood-brain barrier endothelial cell permeability changes induced by hypoxia and posthypoxic reoxygenation.
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The blood-brain barrier (BBB) is a metabolic and physiological barrier important for maintaining brain homeostasis. The aim of this study was to determine the role of PKC activation in BBB paracellular permeability changes induced by hypoxia and posthypoxic reoxygenation using in vitro and in vivo
[The anti-apoptosis effect of erythropoietin on neonatal rat cardiocytes during hypoxia/reoxygenation injury and its possible mechanism].
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OBJECTIVE
To investigate the anti-apoptosis effect of erythropoietin (EPO) on myocardial cells after hypoxia/reoxygenation in vitro, and the relationship among protein kinase C (PKC), the mitochondrial ATP-sensitive potassium (mitoKATP) channel and EPO in the anti-apoptotic signaling
Cortical delta-opioid receptors potentiate K+ homeostasis during anoxia and oxygen-glucose deprivation.
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Central neurons are extremely vulnerable to hypoxic/ischemic insult, which is a major cause of neurologic morbidity and mortality as a consequence of neuronal dysfunction and death. Our recent work has shown that delta-opioid receptor (DOR) is neuroprotective against hypoxic and excitotoxic stress,
Delayed protection of tetramethylpyrazine on neonatal rat cardiomyocytes subjected to anoxia-reoxygenation injury.
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The aim of this study was to investigate the cardioprotective effects and the possible mechanisms of delayed preconditioning induced by tetramethylpyrazine (TMP) in cultured neonatal rat cardiomyocytes subjected to anoxia-reoxygenation injury. Cultured neonatal rat cardiomyocytes were preconditioned
Chronic intermittent hypoxia alters Ca2+ handling in rat cardiomyocytes by augmented Na+/Ca2+ exchange and ryanodine receptor activities in ischemia-reperfusion.
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This study examined Ca(2+) handling mechanisms involved in cardioprotection induced by chronic intermittent hypoxia (CIH) against ischemia-reperfusion (I/R) injury. Adult male Sprague-Dawley rats were exposed to 10% inspired O(2) continuously for 6 h daily from 3, 7, and 14 days. In isolated
[Effects of pioglitazone on mitochondrial membrane potential of neonate rat's myocardial cells after hypoxia/reoxygenation].
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OBJECTIVE
To explore the effectiveness and mechanism of pioglitazone on mitochondrial membrane potential of neonate rat's myocardial cells after hypoxia/reoxygenation.
METHODS
Primary cultured myocardial cells of neonate Sprague-Dawley rats were pretreated with different concentrations of
Exogenous 10 kDa-Heat Shock Protein Preserves Mitochondrial Function After Hypoxia/Reoxygenation
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Humoral factors released during ischemic preconditioning (IPC) protect the myocardium against ischemia/reperfusion (I/R) injury. We have recently identified 10 kDa-heat shock protein (HSP10) and a fraction of small 5-10 kDa peptides (5-10-sP) in the coronary effluent of IPC-treated hearts and
Chronic hypoxia alters fetal cerebrovascular responses to endothelin-1.
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In utero hypoxia influences the structure and function of most fetal arteries, including those of the developing cerebral circulation. Whereas the signals that initiate this hypoxic remodeling remain uncertain, these appear to be distinct from the mechanisms that maintain the remodeled vascular
Effects of desflurane and propofol on electrophysiological parameters during and recovery after hypoxia in rat hippocampal slice CA1 pyramidal cells.
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Cerebral ischemia is a major cause of death and disability and may be a complication of neurosurgery. Certain anesthetics may improve recovery after ischemia and hypoxia by altering electrophysiological changes during the insult. Intracellular recordings were made from CA1 pyramidal cells in
Hypoxia differentially regulates stress proteins in cultured cardiomyocytes: role of the p38 stress-activated kinase signaling cascade, and relation to cytoprotection.
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Stress proteins (heat shock proteins, HSPs) are molecular chaperones that have been shown to enhance the survival of cells exposed to environmental stress. We sought to investigate the effects of hypoxia on the levels of HSP27 and heme oxygenase-1 (HO-1 or HSP32) in an established model of
Hypoxia increases calcium flux through cortical neuron glutamate receptors via protein kinase C.
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The effects of 30 s to 10 min hypoxia (PO2-10 mmHg) on glutamate receptor activity were studied in murine cortical neurons. Receptor activity was assessed as a rise in intracellular calcium concentration ([Ca2+]i) following a 10 s application of 1 mm glutamate or 100 micro mN-methy-d-aspartate
Chronic Intermittent Hypobaric Hypoxia Improves Cardiac Function through Inhibition of Endoplasmic Reticulum Stress.
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We investigated the role of endoplasmic reticulum stress (ERS) in chronic intermittent hypobaric hypoxia (CIHH)-induced cardiac protection. Adult male Sprague-Dawley rats were exposed to CIHH treatment simulating 5000 m altitude for 28 days, 6 hours per day. The heart was isolated and perfused with
Preservation of the pHi during ischemia via PKC by intermittent hypoxia.
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In intermittent hypoxia adaptation (IHA) rat cardiomyocytes, the relationship between activated protein kinase C and intracellular acidification regulation during ischemia-reperfusion (I/R) was tested. Using [H(+)] indicator BCECF-AM, we analyzed the alterations of intracellular pH (pH(i)) in
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