Neuroprotection in Ischemic/Hypoxic Disorders

In the brain, the most common lesion is ischemic and/or hypoxic by origin. The insult results in neuronal loss. The primary aim of therapeutic interventions to reduce the volume of brain damage and thus, to lessen the neurological impairment, disability and handicap among stroke survivors. Reduction in infarct size may also reduce the risk of early death, particularly due to ischemic cerebral edema and transtentorial herniation.

[1]  V. Lakics,et al.  Protection against veratridine toxicity in rat cortical cultures: relationship to sodium channel blockade , 1995, Neuroreport.

[2]  J. Krieglstein,et al.  Pharmacology of cerebral ischemia : proceedings of the International Symposium on Pharmacology of Cerebral Ischemia, held in Marburg (FRG) on 16-17 July 1986 , 1986 .

[3]  H. Katsuki,et al.  Idebenone and vinpocetine augment long-term potentiation in hippocampal slices in the guinea pig , 1989, Neuropharmacology.

[4]  N. van Bruggen,et al.  VEGF antagonism reduces edema formation and tissue damage after ischemia/reperfusion injury in the mouse brain. , 1999, The Journal of clinical investigation.

[5]  C. Sommer,et al.  Selective c‐JUN Expression in CA1 Neurons of the Gerbil Hippocampus during and after Acquisition of an Ischemia‐Tolerant State , 1995, Brain pathology.

[6]  J. Stamler,et al.  Actions of redox-related congeners of nitric oxide at the NMDA receptor , 1994, Neuropharmacology.

[7]  David J Gladstone,et al.  Toward Wisdom From Failure: Lessons From Neuroprotective Stroke Trials and New Therapeutic Directions , 2002, Stroke.

[8]  A. Aguzzi,et al.  Differential Transcription and Translation of Immediate Early Genes in the Gerbil Hippocampus after Transient Global Ischemia , 1993, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[9]  S. Kaneko,et al.  The use of Xenopus oocytes to evaluate drugs affecting brain Ca2+ channels: effects of bifemelane and several nootropic agents. , 1990, European journal of pharmacology.

[10]  M. Fujimura,et al.  Early Appearance of Activated Matrix Metalloproteinase-9 after Focal Cerebral Ischemia in Mice: A Possible Role in Blood—Brain Barrier Dysfunction , 1999, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[11]  M. Miyazaki.  The Effect of a Cerebral Vasodilator, Vinpocetine, on Cerebral Vascular Resistance Evaluated by the Doppler Ultrasonic Technique in Patients with Cerebrovascular Diseases , 1995, Angiology.

[12]  J. LaManna,et al.  Hypoxia-induced brain angiogenesis. Signals and consequences. , 1998, Advances in experimental medicine and biology.

[13]  M Chopp,et al.  Antibodies against Adhesion Molecules Reduce Apoptosis after Transient Middle Cerebral Artery Occlusion in Rat Brain , 1996, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[14]  King Ga.  Protective effects of vinpocetine and structurally related drugs on the lethal consequences of hypoxia in mice. , 1987, Archives internationales de pharmacodynamie et de therapie.

[15]  S. Erdö,et al.  Vinpocetine is as potent as phenytoin to block voltage-gated Na+ channels in rat cortical neurons. , 1995, European journal of pharmacology.

[16]  M. Goldberg,et al.  Sequencing of the human vascular endothelial growth factor (VEGF) 3' untranslated region (UTR): conservation of five hypoxia-inducible RNA-protein binding sites. , 1997, Biochimica et biophysica acta.

[17]  M. Hennerici,et al.  Meta-Analysis of Oral Nimodipine Trials in Acute Ischemic Stroke , 1994 .

[18]  V. Feigin,et al.  Vinpocetine treatment in acute ischaemic stroke: a pilot single‐blind randomized clinical trial , 2001, European journal of neurology.

[19]  M. Chopp,et al.  Induction of DNA fragmentation after 10 to 120 minutes of focal cerebral ischemia in rats. , 1995, Stroke.

[20]  R. Simon,et al.  Ischemic tolerance in the brain , 1997, Neurology.

[21]  H. Budka,et al.  A comparative study on the expression of cyclooxygenase and 5-lipoxygenase during cerebral ischemia in humans , 2002, Acta Neuropathologica.

[22]  M. Ross,et al.  Inducible nitric oxide synthase gene expression in vascular cells after transient focal cerebral ischemia. , 1996, Stroke.

[23]  M. Fujimura,et al.  Early Decrease of Apurinic/Apyrimidinic Endonuclease Expression after Transient Focal Cerebral Ischemia in Mice , 1999, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[24]  K. Welch,et al.  Expression of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 after focal cerebral ischemia in the rat , 1995, Journal of Neuroimmunology.

[25]  J. Skopál,et al.  Expression of membrane-bound and soluble cell adhesion molecules by human brain microvessel endothelial cells. , 1999, Microvascular research.

[26]  V. Lakics,et al.  Vinpocetine is a highly potent neuroprotectant against veratridine-induced cell death in primary cultures of rat cerebral cortex , 1995, Neuroscience Letters.

[27]  L. Zon,et al.  Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosis , 1996, Nature.

[28]  M. Chopp,et al.  Thrombolysis with tissue plasminogen activator alters adhesion molecule expression in the ischemic rat brain. , 1999, Stroke.

[29]  H. Nawashiro,et al.  Inhibition of Tumor Necrosis Factor and Amelioration of Brain Infarction in Mice , 1997, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[30]  J. Koziol,et al.  Matrix Metalloproteinases Increase Very Early during Experimental Focal Cerebral Ischemia , 1999, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[31]  P. Ratcliffe,et al.  Oxygen sensing, hypoxia-inducible factor-1 and the regulation of mammalian gene expression. , 1998, The Journal of experimental biology.

[32]  N. Rothwell,et al.  Cerebral Interleukin-6 is Neuroprotective during Permanent Focal Cerebral Ischemia in the Rat , 1998, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[33]  Jun Chen,et al.  bcl-2 is expressed in neurons that survive focal ischemia in the rat. , 1995, Neuroreport.

[34]  Z. Qin,et al.  Tumor necrosis factor alpha expression produces increased blood-brain barrier permeability following temporary focal cerebral ischemia in mice. , 1999, Brain research. Molecular brain research.

[35]  D. Latchman,et al.  Delivery of a constitutively active form of the heat shock factor using a virus vector protects neuronal cells from thermal or ischaemic stress but not from apoptosis , 1998, The European journal of neuroscience.

[36]  D. Groo,et al.  Effects of vinpocetine in scopolamine‐induced learning and memory impairments , 1987 .

[37]  P. Moreira,et al.  Synaptosomal response to oxidative stress: Effect of vinpocetine , 2000, Free radical research.

[38]  J. Krieglstein,et al.  A mouse model of focal cerebral ischemia for screening neuroprotective drug effects. , 1992, Journal of pharmacological and toxicological methods.

[39]  G. Rosenberg,et al.  Matrix Metalloproteinases in Cerebrovascular Disease , 1998, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[40]  C. N. Coleman,et al.  Salicylic acid and aspirin inhibit the activity of RSK2 kinase and repress RSK2-dependent transcription of cyclic AMP response element binding protein- and NF-kappa B-responsive genes. , 1999, Journal of immunology.

[41]  T. Yue,et al.  Prolonged Expression of Interferon‐Inducible Protein‐10 in Ischemic Cortex After Permanent Occlusion of the Middle Cerebral Artery in Rat , 1998, Journal of neurochemistry.

[42]  N. Futrell,et al.  Gene expression of IL-10 in relationship to TNF-α, IL-1β and IL-2 in the rat brain following middle cerebral artery occlusion , 1997, Journal of the Neurological Sciences.

[43]  J. Krieglstein,et al.  Effects of vinpocetine on local cerebral blood flow and glucose utilization seven days after forebrain ischemia in the rat. , 1990, Pharmacology.

[44]  J. Krieglstein,et al.  Protective effect of vinpocetine against brain damage caused by ischemia. , 1991, Japanese journal of pharmacology.

[45]  R. Schmidt-Kastner,et al.  Cortical spreading depression activates trophic factor expression in neurons and astrocytes and protects against subsequent focal brain ischemia , 1998, Brain Research.

[46]  S. Stolc,et al.  Indole derivatives as neuroprotectants. , 1999, Life sciences.

[47]  G. Semenza,et al.  Induction of hypoxia‐inducible factor‐1 (HIF‐1) and its target genes following focal ischaemia in rat brain , 1999, The European journal of neuroscience.

[48]  L. Tretter,et al.  The neuroprotective drug vinpocetine prevents veratridine‐induced [Na+]i and [Ca2+]i rise in synaptosomes , 1998, Neuroreport.

[49]  T. Nowak.  Localization of 70 kDa Stress Protein mRNA Induction in Gerbil Brain after Ischemia , 1991, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[50]  O. Wiestler,et al.  Expression of the Ets-1 transcription factor in human astrocytomas is associated with Fms-like tyrosine kinase-1 (Flt-1)/vascular endothelial growth factor receptor-1 synthesis and neoangiogenesis. , 1999, Cancer research.

[51]  B. Lendvai,et al.  The Nootropic Drug Vinpocetine Inhibits Veratridine-Induced [Ca2+]i Increase in Rat Hippocampal CA1 Pyramidal Cells , 2001, Neurochemical Research.

[52]  S. Kawabata,et al.  Cerebral vasodilators potentiate the anti-anoxic activity of indeloxazine hydrochloride, a new cerebral activator , 1989, Neuropharmacology.

[53]  A. Nairn,et al.  Glutamate-Dependent Phosphorylation of Elongation Factor-2 and Inhibition of Protein Synthesis in Neurons , 1997, The Journal of Neuroscience.

[54]  D. Groo,et al.  Comparison of the effects of vinpocetine, vincamine, and nicergoline on the normal and hypoxia‐damaged learning process in spontaneously hypertensive rats , 1988 .

[55]  R. Bravo.  Growth factor-responsive genes in fibroblasts. , 1990, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.

[56]  N. Wahlgren.  A review of earlier clinical studies on neuroprotective agents and current approaches. , 1997, International review of neurobiology.

[57]  J. Hallenbeck,et al.  Heat-Shock Protein and C-fos Expression in Focal Microvascular Brain Damage , 1996, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[58]  M. Mattson.  Neuroprotective Signal Transduction: Relevance to Stroke , 1997, Neuroscience & Biobehavioral Reviews.

[59]  T. Ohtsuka,et al.  Expression of Interleukin-1β Converting Enzyme Gene Family and bcl-2 Gene Family in the Rat Brain following Permanent Occlusion of the Middle Cerebral Artery , 1997, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[60]  Kevin K. W Wang,et al.  Calpain and caspase: can you tell the difference? , 2000, Trends in Neurosciences.

[61]  C. Iadecola.  Bright and dark sides of nitric oxide in ischemic brain injury , 1997, Trends in Neurosciences.

[62]  H. Hara,et al.  Protective effect of KB-2796, a new calcium antagonist, in cerebral hypoxia and ischemia. , 1990, Archives internationales de pharmacodynamie et de therapie.

[63]  M. Moskowitz,et al.  Effects of cerebral ischemia in mice deficient in neuronal nitric oxide synthase. , 1994, Science.

[64]  Z. Dong,et al.  Antioxidant properties of aspirin: Characterization of the ability of aspirin to inhibit silica-induced lipid peroxidation, DNA damage, NF-κB activation, and TNF-α production , 2004, Molecular and Cellular Biochemistry.

[65]  Blair R. Leavitt,et al.  Induction of neurogenesis in the neocortex of adult mice , 2000, Nature.

[66]  N. Wood,et al.  Differential expression of c-fos, Hsp70 and Hsp27 after photothrombotic injury in the rat brain. , 1997, Brain research. Molecular brain research.

[67]  S. Vannucci,et al.  Coordinate IGF-I and IGFBP5 Gene Expression in Perinatal Rat Brain after Hypoxia-Ischemia , 1996, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[68]  J. D. Macklis,et al.  Induction of neuronal type-specific neurogenesis in the cerebral cortex of adult mice: manipulation of neural precursors in situ. , 2002, Brain research. Developmental brain research.

[69]  M. Moskowitz,et al.  Activation and Cleavage of Caspase-3 in Apoptosis Induced by Experimental Cerebral Ischemia , 1998, The Journal of Neuroscience.

[70]  M. Chopp,et al.  In situ detection of DNA fragmentation after focal cerebral ischemia in mice. , 1995, Brain Research. Molecular Brain Research.

[71]  D. Ferriero,et al.  Hypoxia-Ischemia, but Not Hypoxia Alone, Induces the Expression of Heme Oxygenase-1 (HSP32) in Newborn Rat Brain , 1997, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[72]  W. Risau,et al.  HRF, a putative basic helix-loop-helix-PAS-domain transcription factor is closely related to hypoxia-inducible factor-1α and developmentally expressed in blood vessels , 1997, Mechanisms of Development.

[73]  T. Curran,et al.  Stimulus-transcription coupling in the nervous system: involvement of the inducible proto-oncogenes fos and jun. , 1991, Annual review of neuroscience.

[74]  R. Voellmy,et al.  Repression of Heat Shock Transcription Factor HSF1 Activation by HSP90 (HSP90 Complex) that Forms a Stress-Sensitive Complex with HSF1 , 1998, Cell.

[75]  M. Kennedy,et al.  The major tyrosine-phosphorylated protein in the postsynaptic density fraction is N-methyl-D-aspartate receptor subunit 2B. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[76]  M. Moskowitz,et al.  Pathobiology of ischaemic stroke: an integrated view , 1999, Trends in Neurosciences.

[77]  G. Semenza.  Perspectives on Oxygen Sensing , 1999, Cell.

[78]  J. Beckman.  Nitric Oxide, Superoxide, and Peroxynitrite in CNS Injury , 1997 .

[79]  M. Chopp,et al.  Neuronal survival is associated with 72-kDa heat shock protein expression after transient middle cerebral artery occlusion in the rat , 1993, Journal of the Neurological Sciences.

[80]  John Garthwaite,et al.  Interaction of the antiepileptic drug lamotrigine with recombinant rat brain type IIA Na+ channels and with native Na+ channels in rat hippocampal neurones , 1995, Pflügers Archiv.

[81]  V. Denoble.  Vinpocetine enhances retrieval of a step-through passive avoidance response in rats , 1987, Pharmacology Biochemistry and Behavior.

[82]  C. Cobbs,et al.  Vascular endothelial growth factor expression in transient focal cerebral ischemia in the rat , 1998, Neuroscience Letters.

[83]  M. Dragunow,et al.  Neuronal death and survival in two models of hypoxic-ischemic brain damage , 1999, Brain Research Reviews.

[84]  R. Sapolsky,et al.  Gene therapy with HSP72 is neuroprotective in rat models of stroke and epilepsy , 1998, Annals of neurology.

[85]  M. Ross,et al.  The Cyclooxygenase-2 Inhibitor NS-398 Ameliorates Ischemic Brain Injury in Wild-Type Mice but not in Mice with Deletion of the Inducible Nitric Oxide Synthase Gene , 1999, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[86]  K. Kogure,et al.  Comparative neuroprotective effects of pentobarbital, vinpocetine, flunarizine and ifenprodil on ischemic neuronal damage in the gerbil hippocampus , 1990, Research in experimental medicine. Zeitschrift fur die gesamte experimentelle Medizin einschliesslich experimenteller Chirurgie.

[87]  T. Sugawara,et al.  Early decrease of XRCC1, a DNA base excision repair protein, may contribute to DNA fragmentation after transient focal cerebral ischemia in mice. , 1999, Stroke.

[88]  T. Curran,et al.  Immediate-early genes: ten years on , 1995, Trends in Neurosciences.

[89]  T. Yanagihara,et al.  Alterations of Bcl-2 family proteins precede cytoskeletal proteolysis in the penumbra, but not in infarct centres following focal cerebral ischemia in mice , 1998, Neuroscience.

[90]  M. Chopp,et al.  Protein Expression and Brain Plasticity After Transient Middle Cerebral Artery Occlusion in the Rat , 1999 .