ArticleAnnual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference2019
Neuroprotection of Glibenclamide against Brain Injury after Cardiac Arrest via Modulation of NLRP3 Inflammasome.
Article in Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Hemoglobin vesicles improve neurological outcomes after cardiac arrest in rats.Resuscitation plus · 2024Article
- Impact of Antidiabetic Drugs on Clinical Outcomes of COVID-19: A Nationwide Population-Based Study.Endocrinology and metabolism (Seoul, Korea) · 2024Article
- Neuroprotection of NSC Therapy is Superior to Glibenclamide in Cardiac Arrest-Induced Brain Injury via Neuroinflammation Regulation.Translational stroke research · 2023Article
- Targeting of neuroinflammation by glibenclamide in Covid-19: old weapon from arsenal.Inflammopharmacology · 2023Review
- Pharmacological Approach for Neuroprotection After Cardiac Arrest-A Narrative Review of Current Therapies and Future Neuroprotective Cocktail.Frontiers in medicine · 2021Review
- Progesterone Attenuates Stress-Induced NLRP3 Inflammasome Activation and Enhances Autophagy following Ischemic Brain Injury.International journal of molecular sciences · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Glibenclamide (GBC) improves cerebral outcome after cardiac arrest (CA) in rats. We aim to investigate the effect of GBC on electrophysiological recovery and to explore the mechanism of neuroprotective effects of GBC on the acute stage of brain injury after the return of spontaneous circulation (ROSC) in a rodent model of CA. 16 anesthetized male Wistar rats subjected to 8-min asphyxia-CA were randomly assigned to the GBC or control group (N=8 each group). GBC was administered with a loading dose of 10ug/kg i. p. injection 10 min after ROSC and followed with a maintaining dose of 1.6ug/kg per 8 hours throughout the first 24 hours. Quantitative measures of EEG-information quantity (qEEG-IQ) and neurological deficit score (NDS) were used to predict and evaluate the functional outcome. There was a significant improvement of NDS in rats treated with GBC compared with the control group (p <; 0.01). Compared to the control group, the rats treated with GBC showed qEEG-IQ scores that indicated better recovery (p <; 0.001). Meanwhile, early QEEG-IQ was significantly correlated with 72-hr NDS as early as 45min after ROSC. Furthermore, on the molecular basis, the NLRP3 inflammasome was strongly activated in the hippocampal CA1 area 3 days after CA in control rats, which was suppressed with GBC treatment. Taken together, GBC treatment markedly improved electrophysiological and neurologic outcomes of the acute brain injury after CA. These neuroprotective effects may be associated with the attenuation of inflammatory response via down-regulation of NLRP3 inflammasome signal.
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