• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

Autophagy Mediates Astrocyte Death During Zinc-Potentiated Ischemia-Reperfusion Injury.
Abstract Pathological release of excess zinc ions and the resultant increase in intracellular zinc has been implicated in ischemic brain cell death, although the underlying mechanisms are not fully understood. Since zinc promotes the formation of the autophagic signal, reactive oxygen species (ROS), and increases autophagy, a known mechanism of cell death, we hypothesized that autophagy is involved in zinc-induced hypoxic cell death. To study this hypothesis, we determined the effect of zinc on autophagy and ROS generation in C8-D1A astrocytes subjected to hypoxia and rexoygenation (H/R), simulating ischemic strok...
Source: Biological Trace Element Research - March 12, 2015 Category: Biology Authors: Pan R, Timmins GS, Liu W, Liu KJ Tags: Biol Trace Elem Res Source Type: research

Indomethacin preconditioning induces ischemic tolerance by modifying zinc availability in the brain.
This study found that chronic pretreatment of rats with indomethacin, a non-selective cyclooxygenase inhibitor, provided tolerance to ischemic injuries in an animal model of stroke by eliciting moderate zinc elevation in neurons. Consecutive intraperitoneal injection of indomethacin (3mg/kg/day for 28days) led to modest increases in intraneuronal zinc as well as synaptic zinc content, with no significant stimulation of neuronal death. Furthermore, indomethacin induced the expression levels of intracellular zinc homeostatic and neuroprotective proteins, rendering the brain resistant against ischemic damages and improving ne...
Source: Neurobiology of Disease - January 3, 2015 Category: Neurology Authors: Lee J, Oh SB, Hwang J, Suh N, Jo D, Kim JS, Koh J Tags: Neurobiol Dis Source Type: research

Zinc Promotes the Death of Hypoxic Astrocytes by Upregulating Hypoxia-Induced Hypoxia-Inducible Factor-1alpha Expression via Poly(ADP-ribose) Polymerase-1.
CONCLUSIONS: Our studies show that zinc promotes hypoxic cell death through overexpression of the hypoxia response factor HIF-1α via the cell fate determine factor PARP-1 modification, which provides a novel mechanism for zinc-mediated ischemic brain injury. PMID: 23582235 [PubMed - as supplied by publisher]
Source: CNS Neuroscience and Therapeutics - April 13, 2013 Category: Neuroscience Authors: Pan R, Chen C, Liu WL, Liu KJ Tags: CNS Neurosci Ther Source Type: research

Pages: 1  2  3  4  5  6