ArticleJournal of neurochemistry2003
Assessment of the relative contribution of COX-1 and COX-2 isoforms to ischemia-induced oxidative damage and neurodegeneration following transient global cerebral ischemia.
Article in Journal of neurochemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 183 citations in OpenAlex.
- Oxidative Stress in Health and Disease: Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Does Administration of Low-Dose Aspirin Enhance the Efficacy of Psychotropic Drugs in Patients with Bipolar Disorder, Schizophrenia, and Schizoaffective Disorder?Pharmaceuticals (Basel, Switzerland) · 2026Article
- Glucagon-like peptide-1: a multi-faceted anti-inflammatory agent.Frontiers in immunology · 2023Review
- Liver X Receptor as a Possible Drug Target for Blood-Brain Barrier Integrity.Advanced pharmaceutical bulletin · 2022Review
- COX-2/PGE2 Pathway Inhibits the Ferroptosis Induced by Cerebral Ischemia Reperfusion.Molecular neurobiology · 2022Article
- Genetic Deletion or Pharmacological Inhibition of Cyclooxygenase-2 Reduces Blood-Brain Barrier Damage in Experimental Ischemic Stroke.Frontiers in neurology · 2020Article
- Neuroinflammation: friend and foe for ischemic stroke.Journal of neuroinflammation · 2019Review
- Combining anti-inflammatory and unfolding protein responses to fight stroke.Neural regeneration research · 2019Article
- Immunomodulatory Therapeutic Strategies in Stroke.Frontiers in pharmacology · 2019Review
- MiR-21b-3p protects NS2OY cells against oxygen-glucose deprivation/reperfusion-induced injury by down-regulating cyclooxygenase-2.American journal of translational research · 2019Article
- Anti-inflammatory Effect of Glucagon Like Peptide-1 Receptor Agonist, Exendin-4, through Modulation of IB1/JIP1 Expression and JNK Signaling in Stroke.Experimental neurobiology · 2017 · on this mapArticle
- The potential neuroprotective role of a histone deacetylase inhibitor, sodium butyrate, after neonatal hypoxia-ischemia.Journal of neuroinflammation · 2017Article
- Treatment Effects of Ischemic Stroke by Berberine, Baicalin, and Jasminoidin from Huang-Lian-Jie-Du-Decoction (HLJDD) Explored by an Integrated Metabolomics Approach.Oxidative medicine and cellular longevity · 2017Article
- Mesenchymal Stem Cell-Derived Extracellular Vesicles Ameliorates Hippocampal Synaptic Impairment after Transient Global Ischemia.Frontiers in cellular neuroscience · 2017Article
- Functional magnetic resonance imaging in chronic ischaemic stroke.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- Contribution of prostanoid signaling to the evolution of spreading depolarization and the associated cerebral blood flow response.Scientific reports · 2016Article
- Picroside II Inhibits the MEK-ERK1/2-COX2 Signal Pathway to Prevent Cerebral Ischemic Injury in Rats.Journal of molecular neuroscience : MN · 2015Article
- Phospholipid scramblase 1 is required for β2-glycoprotein I binding in hypoxia and reoxygenation-induced endothelial inflammation.Journal of leukocyte biology · 2015Article
- TAK-242, an antagonist for Toll-like receptor 4, protects against acute cerebral ischemia/reperfusion injury in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
- 12/15-Lipoxygenase metabolites of arachidonic acid activate PPARγ: a possible neuroprotective effect in ischemic brain.Journal of lipid research · 2015Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
We investigated the relative contribution of COX-1 and/or COX-2 to oxidative damage, prostaglandin E2 (PGE2) production and hippocampal CA1 neuronal loss in a model of 5 min transient global cerebral ischemia in gerbils. Our results revealed a biphasic and significant increase in PGE2 levels after 2 and 24-48 h of reperfusion. The late increase in PGE2 levels (24 h) was more potently reduced by the highly selective COX-2 inhibitor rofecoxib (20 mg/kg) relative to the COX-1 inhibitor valeryl salicylate (20 mg/kg). The delayed rise in COX catalytic activity preceded the onset of histopathological changes in the CA1 subfield of the hippocampus. Post-ischemia treatment with rofecoxib (starting 6 h after restoration of blood flow) significantly reduced measures of oxidative damage (glutathione depletion and lipid peroxidation) seen at 48 h after the initial ischemic episode, indicating that the late increase in COX-2 activity is involved in the delayed occurrence of oxidative damage in the hippocampus after global ischemia. Interestingly, either selective inhibition of COX-2 with rofecoxib or inhibition of COX-1 with valeryl salicylate significantly increased the number of healthy neurons in the hippocampal CA1 sector even when the treatment began 6 h after ischemia. These results provide the first evidence that both COX isoforms are involved in the progression of neuronal damage following global cerebral ischemia, and have important implications for the potential therapeutic use of COX inhibitors in cerebral ischemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.