Effect of Bradykinin Postconditioning on Ischemic and Toxic Brain Damage
暂无分享,去创建一个
[1] Ying Zhu,et al. Prosurvival NMDA 2A receptor signaling mediates postconditioning neuroprotection in the hippocampus , 2015, Hippocampus.
[2] J. Burda,et al. Delayed post-conditioning reduces post-ischemic glutamate level and improves protein synthesis in brain , 2013, Neurochemistry International.
[3] Jiyao Jiang,et al. Neuroprotective effects of ischemic postconditioning on global brain ischemia in rats through upregulation of hippocampal glutamine synthetase , 2011, Journal of Clinical Neuroscience.
[4] S. Sakoda,et al. Activation of NR2A Receptors Induces Ischemic Tolerance through CREB Signaling , 2010, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[5] R. Bordet,et al. Sevoflurane pre- and post-conditioning protect the brain via the mitochondrial K ATP channel. , 2010, British journal of anaesthesia.
[6] Eun Ki Kim,et al. Inhibitory Effect of Poncirus trifoliate on Acetylcholinesterase and Attenuating Activity against Trimethyltin-Induced Learning and Memory Impairment , 2009, Bioscience, biotechnology, and biochemistry.
[7] Takahiro Shimizu,et al. Bradykinin‐induced astrocyte–neuron signalling: glutamate release is mediated by ROS‐activated volume‐sensitive outwardly rectifying anion channels , 2009, The Journal of physiology.
[8] J. Burda,et al. Transient Forebrain Ischemia Impact on Lymphocyte DNA Damage, Glutamic Acid Level, and SOD Activity in Blood , 2009, Cellular and Molecular Neurobiology.
[9] J. Burda,et al. Postconditioning and Anticonditioning: Possibilities to Interfere to Evoked Apoptosis , 2009, Cellular and Molecular Neurobiology.
[10] G. Niu,et al. Delayed Postconditioning Protects against Focal Ischemic Brain Injury in Rats , 2008, PloS one.
[11] Z. Hliňák,et al. Dipeptide "alaptide" prevented impairments in spontaneous behavior produced with trimethyltin in male rats. , 2008, Neuro endocrinology letters.
[12] R. Bordet,et al. Preconditioning by an in situ administration of hydrogen peroxide: Involvement of reactive oxygen species and mitochondrial ATP-dependent potassium channel in a cerebral ischemia–reperfusion model , 2008, Brain Research.
[13] Chonggang Wang,et al. Acute trimethyltin exposure induces oxidative stress response and neuronal apoptosis in Sebastiscus marmoratus. , 2008, Aquatic toxicology.
[14] Mary P. Stenzel-Poore,et al. Mechanisms of ischemic brain damage , 2008, Neuropharmacology.
[15] Xuwen Gao,et al. Protective effects of ischemic postconditioning compared with gradual reperfusion or preconditioning , 2008, Journal of neuroscience research.
[16] Min Zhang,et al. Ischemic Postconditioning Inhibits Apoptosis After Focal Cerebral Ischemia/Reperfusion Injury in the Rat , 2008, Stroke.
[17] B. Luo,et al. Ischemic Postconditioning Protects Against Global Cerebral Ischemia/Reperfusion-Induced Injury in Rats , 2008, Stroke.
[18] J. Burda,et al. Effects of Bradykinin Postconditioning on Endogenous Antioxidant Enzyme Activity After Transient Forebrain Ischemia in Rat , 2008, Neurochemical Research.
[19] J. S. King,et al. Preconditioning Reprograms the Response to Ischemic Injury and Primes the Emergence of Unique Endogenous Neuroprotective Phenotypes: A Speculative Synthesis , 2007, Stroke.
[20] J. Borowitz,et al. Trimethyltin-induced apoptosis is associated with upregulation of inducible nitric oxide synthase and Bax in a hippocampal cell line. , 2006, Toxicology and applied pharmacology.
[21] J. Burda,et al. The Changes in Endogenous Antioxidant Enzyme Activity After Postconditioning , 2006, Cellular and Molecular Neurobiology.
[22] J. Burda,et al. Delayed Postconditionig Initiates Additive Mechanism Necessary for Survival of Selectively Vulnerable Neurons After Transient Ischemia in Rat Brain , 2006, Cellular and Molecular Neurobiology.
[23] K. Reuhl,et al. Trimethyltin-induced alterations in behavior are linked to changes in PSA-NCAM expression. , 2006, Neurotoxicology.
[24] D. Lumenta,et al. Neuroprotective effects of a postischemic treatment with a bradykinin B2 receptor antagonist in a rat model of temporary focal cerebral ischemia , 2006, Brain Research.
[25] O. Hurtado,et al. In Vitro Ischemic Tolerance Involves Upregulation of Glutamate Transport Partly Mediated by the TACE/ADAM17-Tumor Necrosis Factor-α Pathway , 2004, The Journal of Neuroscience.
[26] N. Abbott. Inflammatory Mediators and Modulation of Blood–Brain Barrier Permeability , 2000, Cellular and Molecular Neurobiology.
[27] D. Busija,et al. Diazoxide induces delayed pre‐conditioning in cultured rat cortical neurons , 2003, Journal of neurochemistry.
[28] B. Palmier,et al. LF 16‐0687 Ms, a bradykinin B2 receptor antagonist, reduces ischemic brain injury in a murine model of transient focal cerebral ischemia , 2003, British journal of pharmacology.
[29] E. Uhl,et al. Bradykinin Antagonists Reduce Leukocyte–Endothelium Interactions after Global Cerebral Ischemia , 2003, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[30] E. Ling,et al. Nitric oxide induces macrophage apoptosis following traumatic brain injury in rats , 2003, Neuroscience Letters.
[31] D. Lumenta,et al. Effects of LF 16-0687 Ms, a bradykinin B2 receptor antagonist, on brain edema formation and tissue damage in a rat model of temporary focal cerebral ischemia , 2002, Brain Research.
[32] D. Busija,et al. MitoKATP opener, diazoxide, reduces neuronal damage after middle cerebral artery occlusion in the rat , 2002 .
[33] R. House,et al. Preventable exposure to trimethyl tin chloride: a case report. , 2002, Occupational medicine.
[34] M. Mattson,et al. Activation of Mitochondrial ATP-Dependent Potassium Channels Protects Neurons against Ischemia-Induced Death by a Mechanism Involving Suppression of Bax Translocation and Cytochrome c Release , 2002, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[35] D. Busija,et al. MitoK(ATP) opener, diazoxide, reduces neuronal damage after middle cerebral artery occlusion in the rat. , 2002, American journal of physiology. Heart and circulatory physiology.
[36] P. Chan,et al. Free radical pathways in CNS injury. , 2000, Journal of neurotrauma.
[37] A. K. Chow,et al. Preconditioning with Cortical Spreading Depression Decreases Intraischemic Cerebral Glutamate Levels and Down‐Regulates Excitatory Amino Acid Transporters EAAT1 and EAAT2 from Rat Cerebal Cortex Plasma Membranes , 2000, Journal of neurochemistry.
[38] B. Meldrum,et al. Glutamate as a neurotransmitter in the brain: review of physiology and pathology. , 2000, The Journal of nutrition.
[39] Philip Wexler,et al. Toxnet: A computerized collection of toxicological and environmental health information , 2000, Toxicology and industrial health.
[40] J. Downey,et al. Signal Transduction in Ischemic Preconditioning: , 1999, Journal of cardiovascular electrophysiology.
[41] A. Doble. The role of excitotoxicity in neurodegenerative disease: implications for therapy. , 1999 .
[42] C. Sobey,et al. Mechanisms of bradykinin-induced cerebral vasodilatation in rats. Evidence that reactive oxygen species activate K+ channels. , 1997, Stroke.
[43] Y. Watanabe,et al. Trimethyltin syndrome as a hippocampal degeneration model: temporal changes and neurochemical features of seizure susceptibility and learning impairment , 1997, Neuroscience.
[44] A. Unterberg,et al. Vasomotor and permeability effects of bradykinin in the cerebral microcirculation. , 1996, Immunopharmacology.
[45] M. Billingsley,et al. Induction of apoptosis by organotin compounds in vitro: neuronal protection with antisense oligonucleotides directed against stannin. , 1996, The Journal of pharmacology and experimental therapeutics.
[46] W. Linz,et al. Role of kinins in myocardial ischemia. , 1996, EXS.
[47] Kristina J. Liu,et al. Report of two cases , 1995 .
[48] J. Downey,et al. Role of bradykinin in protection of ischemic preconditioning in rabbit hearts. , 1995, Circulation research.
[49] J. Nadler,et al. The neuroprotective agent riluzole inhibits release of glutamate and aspartate from slices of hippocampal area CA1. , 1993, European journal of pharmacology.
[50] R. Busto,et al. Changes in Amino Acid Neurotransmitters and Cerebral Blood Flow in the Ischemic Penumbral Region following Middle Cerebral Artery Occlusion in the Rat: Correlation with Histopathology , 1993, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[51] Y. Katayama,et al. The Role of Bradykinin in Mediating Ischemic Brain Edema in Rats , 1993, Stroke.
[52] H. Benveniste. The excitotoxin hypothesis in relation to cerebral ischemia. , 1991, Cerebrovascular and brain metabolism reviews.
[53] D. Attwell,et al. The release and uptake of excitatory amino acids. , 1990, Trends in pharmacological sciences.
[54] U. Ungerstedt,et al. Dynamics of Extracellular Metabolites in the Striatum after Middle Cerebral Artery Occlusion in the Rat Monitored by Intracerebral Microdialysis , 1989, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[55] D. Choi,et al. Pharmacology of glutamate neurotoxicity in cortical cell culture: attenuation by NMDA antagonists , 1988, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[56] W. Rosenblum. Hydroxyl Radical Mediates the Endothelium‐Dependent Relaxation Produced by Bradykinin in Mouse Cerebral Arterioles , 1987, Circulation research.
[57] T. J. Walsh,et al. On the role of seizure activity in the hippocampal damage produced by trimethyltin , 1986, Brain Research.
[58] H. Benveniste,et al. Elevation of the Extracellular Concentrations of Glutamate and Aspartate in Rat Hippocampus During Transient Cerebral Ischemia Monitored by Intracerebral Microdialysis , 1984, Journal of neurochemistry.
[59] G. Fagg,et al. Amino acid neurotransmitters and their pathways in the mammalian central nervous system , 1983, Neuroscience.
[60] Fred Plum,et al. Temporal profile of neuronal damage in a model of transient forebrain ischemia , 1982, Annals of neurology.
[61] T. J. Walsh,et al. The trimethyltin syndrome in rats. , 1982, Neurobehavioral toxicology and teratology.
[62] W. D. Ross,et al. Neurotoxic effects of occupational exposure to organotins. , 1981, The American journal of psychiatry.
[63] R. H. Evans,et al. Excitatory amino acid transmitters. , 1981, Annual review of pharmacology and toxicology.
[64] J. Brierley,et al. A New Model of Bilateral Hemispheric Ischemia in the Unanesthetized Rat , 1979, Stroke.
[65] C. Barnes. Memory deficits associated with senescence: a neurophysiological and behavioral study in the rat. , 1979, Journal of comparative and physiological psychology.
[66] E Fortemps,et al. Trimethyltin poisoning · report of two cases , 1978, International archives of occupational and environmental health.
[67] M. M. Bradford. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. , 1976, Analytical biochemistry.
[68] M. H. Aprison,et al. Fluorometric determination of aspartate, glutamate, and γ-aminobutyrate in nerve tissue using enzymic method☆ , 1966 .
[69] M. H. Aprison,et al. Fluorometric determination of aspartate, glutamate, and gamma-aminobutyrate in nerve tissue using enzymic methods. , 1966, Analytical biochemistry.
[70] D. R. Curtis,et al. Analogues of Glutamic and γ-Amino-n-butyric acids having Potent Actions on Mammalian Neurones , 1961, Nature.
[71] D. R. Curtis,et al. Chemical transmitter substances in brain stem of cat. , 1961, Journal of neurophysiology.
[72] D. R. Curtis,et al. The chemical excitation of spinal neurones by certain acidic amino acids , 1960, The Journal of physiology.