naloxone and Brain-Infarction

naloxone has been researched along with Brain-Infarction* in 1 studies

Other Studies

1 other study(ies) available for naloxone and Brain-Infarction

Article	Year
Effect of naloxone on the induction of immediately early genes following oxygen- and glucose-deprivation in PC12 cells. Neuroscience letters, 2008, Jun-20, Volume: 438, Issue:2 Cerebral ischemia/reperfusion involves inflammatory process and naloxone is able to reduce infarct volume and has been used as a therapeutic agent for brain injury. Hypoxia induces the immediate early genes (IEGs) rapidly and transiently that may initiate a cascade of cellular responses that are necessary for survival and normal function. However, the protective effect of naloxone on ischemic/hypoxic neuronal cells was only partly studied. Thus, the effects of naloxone on oxygen- and glucose-deprivation (OGD) and OGD followed by reoxygenation (OGD/R) on the expression of IEGs were examined in PC12 cells. The result showed that lactate dehydrogenase (LDH) released in the media was reduced by naloxone. The temporal response of IEG mRNA encoding c-fos, c-jun, nur77, and zif268 was induced with different degree of intensity following hypoxia, whereas the level of GAPDH mRNA was relatively constant. However, these signals of c-fos, c-jun, and nur77 by hypoxia were reduced significantly by naloxone. Treatment with OGD also activated mitogen-activated protein kinase (MAPK) pathway. The induction of c-fos, c-jun, nur77, and zif268 by hypoxia was inhibited by naloxone (0.1 microM) and MAPK inhibitors (10 microM of U0126, D98059, SB203580). However, naloxone increased the expression of ERK1/2 by OGD concomitantly diminished the LDH release. Thus, the present studies demonstrated that OGD induced IEGs including c-fos, c-jun, nur77, and zif268 and MAPK signaling pathways were regulated differently by naloxone. Topics: Animals; Brain Infarction; Cytoprotection; DNA-Binding Proteins; Encephalitis; Enzyme Inhibitors; Gene Expression Regulation; Genes, Immediate-Early; Hypoxia-Ischemia, Brain; L-Lactate Dehydrogenase; MAP Kinase Signaling System; Mitogen-Activated Protein Kinase 3; Naloxone; Narcotic Antagonists; Neurons; Neuroprotective Agents; Nuclear Receptor Subfamily 4, Group A, Member 1; Oxidative Stress; PC12 Cells; Proto-Oncogene Proteins c-fos; Proto-Oncogene Proteins c-jun; Rats; Receptors, Steroid; Reperfusion Injury	2008

Article

Year

Effect of naloxone on the induction of immediately early genes following oxygen- and glucose-deprivation in PC12 cells.

Neuroscience letters, 2008, Jun-20, Volume: 438, Issue:2

Cerebral ischemia/reperfusion involves inflammatory process and naloxone is able to reduce infarct volume and has been used as a therapeutic agent for brain injury. Hypoxia induces the immediate early genes (IEGs) rapidly and transiently that may initiate a cascade of cellular responses that are necessary for survival and normal function. However, the protective effect of naloxone on ischemic/hypoxic neuronal cells was only partly studied. Thus, the effects of naloxone on oxygen- and glucose-deprivation (OGD) and OGD followed by reoxygenation (OGD/R) on the expression of IEGs were examined in PC12 cells. The result showed that lactate dehydrogenase (LDH) released in the media was reduced by naloxone. The temporal response of IEG mRNA encoding c-fos, c-jun, nur77, and zif268 was induced with different degree of intensity following hypoxia, whereas the level of GAPDH mRNA was relatively constant. However, these signals of c-fos, c-jun, and nur77 by hypoxia were reduced significantly by naloxone. Treatment with OGD also activated mitogen-activated protein kinase (MAPK) pathway. The induction of c-fos, c-jun, nur77, and zif268 by hypoxia was inhibited by naloxone (0.1 microM) and MAPK inhibitors (10 microM of U0126, D98059, SB203580). However, naloxone increased the expression of ERK1/2 by OGD concomitantly diminished the LDH release. Thus, the present studies demonstrated that OGD induced IEGs including c-fos, c-jun, nur77, and zif268 and MAPK signaling pathways were regulated differently by naloxone.

Topics: Animals; Brain Infarction; Cytoprotection; DNA-Binding Proteins; Encephalitis; Enzyme Inhibitors; Gene Expression Regulation; Genes, Immediate-Early; Hypoxia-Ischemia, Brain; L-Lactate Dehydrogenase; MAP Kinase Signaling System; Mitogen-Activated Protein Kinase 3; Naloxone; Narcotic Antagonists; Neurons; Neuroprotective Agents; Nuclear Receptor Subfamily 4, Group A, Member 1; Oxidative Stress; PC12 Cells; Proto-Oncogene Proteins c-fos; Proto-Oncogene Proteins c-jun; Rats; Receptors, Steroid; Reperfusion Injury

2008