ArticleNeurocritical care2018
Glibenclamide Prevents Water Diffusion Abnormality in the Brain After Cardiac Arrest in Rats.
Article in Neurocritical care, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 29 citations in OpenAlex.
- ROS-regulated SUR1-TRPM4 drives persistent activation of NLRP3 inflammasome in microglia after whole-brain radiation.Acta neuropathologica communications · 2025Article
- Evolution of brain injury and neurological dysfunction after cardiac arrest in the rat - A multimodal and comprehensive model.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Neuroprotective Approaches for Brain Injury After Cardiac Arrest: Current Trends and Prospective Avenues.Journal of stroke · 2024Review
- Neuroprotection of NSC Therapy is Superior to Glibenclamide in Cardiac Arrest-Induced Brain Injury via Neuroinflammation Regulation.Translational stroke research · 2023Article
- Research progress on pleiotropic neuroprotective drugs for traumatic brain injury.Frontiers in pharmacology · 2023Review
- Glibenclamide Directly Prevents Neuroinflammation by Targeting SUR1-TRPM4-Mediated NLRP3 Inflammasome Activation In Microglia.Molecular neurobiology · 2022Article
- Flufenamic acid improves survival and neurologic outcome after successful cardiopulmonary resuscitation in mice.Journal of neuroinflammation · 2022Article
- The effect of Glibenclamide on somatosensory evoked potentials after cardiac arrest in rats.Neurocritical care · 2022Article
- Umuhengerin Neuroprotective Effects in Streptozotocin-Induced Alzheimer's Disease Mouse Model via Targeting Nrf2 and NF-Kβ Signaling Cascades.Antioxidants (Basel, Switzerland) · 2021Article
- Article
- Sulfonylurea Receptor 1 in Central Nervous System Injury: An Updated Review.International journal of molecular sciences · 2021Review
- Effect of the KCa3.1 blocker, senicapoc, on cerebral edema and cardiovascular function after cardiac arrest - A randomized experimental rat study.Resuscitation plus · 2021Article
- NLRP3 inflammasome-mediated microglial pyroptosis is critically involved in the development of post-cardiac arrest brain injury.Journal of neuroinflammation · 2020Article
- Role of Sulfonylurea Receptor 1 and Glibenclamide in Traumatic Brain Injury: A Review of the Evidence.International journal of molecular sciences · 2020Review
- Improvement of autistic-like behaviors in adult rats prenatally exposed to valproic acid through early suppression of NMDA receptor function.Psychopharmacology · 2020Article
- BIIB093 (IV glibenclamide): an investigational compound for the prevention and treatment of severe cerebral edema.Expert opinion on investigational drugs · 2019Review
- Neuroprotection of Glibenclamide against Brain Injury after Cardiac Arrest via Modulation of NLRP3 Inflammasome.Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGlibenclamide (GBC) improves neurological outcome after cardiac arrest (CA) in rats. In this study, we sought to elucidate the mechanism responsible for the neuroprotective effects of GBC by using a high-field MRI system.
methodsMale Sprague-Dawley rats were subjected to 10-min asphyxial CA followed by cardiopulmonary resuscitation (CPR). Diffusion-weighted imaging (DWI) as well as conventional T2-weighted imaging was conducted prior to CA and at 24, 48, and 72 h after resuscitation. Afterward, histological examination was performed.
resultsTwelve rats were randomized to receive GBC (n = 6) or vehicle (n = 6) at 15 min after return of spontaneous circulation, while four rats were set as sham control. Rats that underwent CA/CPR and received vehicle exhibited distinct neurological deficit, which was alleviated by GBC treatment. Marked water diffusion abnormality as demonstrated by hyperintense DWI in vulnerable regions of the brain was detected after CA/CPR, with the most prominent hyperintense DWI observed in the hippocampal CA1 region at 72 h. Consistently, histological examination revealed neuronal swelling, dendritic injury, and activation of astrocytes and microglia in the hippocampal CA1 region in vehicle-treated rats. Correlation analysis revealed that the ADC values in the hippocampus were significantly correlated with the histological findings (all p < 0.05).
conclusionThese results suggest that the neuroprotective effects of GBC after CA was exerted, as least in part, through prevention of water diffusion abnormality, namely brain edema.
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