ArticleDrug design, development and therapy2025
Remimazolam Suppresses Oxidative Stress and Apoptosis in Cerebral Ischemia/Reperfusion Injury by Regulating AKT/GSK-3β/NRF2 Pathway.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
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Who cites it
11 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The delirium dichotomy of remimazolam: a differential risk profile for emergence delirium versus postoperative delirium in surgical patients: a systematic review and meta-analysis.Frontiers in medicine · 2026Pooled it
- Association of remimazolam with delirium and cognitive function in elderly patients undergoing general anesthesia or procedural sedation: a meta-analysis of randomized controlled trials.Frontiers in medicine · 2025Pooled it
- Remimazolam Reduces the Cough Reflexes in Elderly Patients Undergoing Fiberoptic Bronchoscopy Under Remifentanil/Cipepofol-Based Anaesthesia: A Randomized Clinical Trial.Drug design, development and therapy · 2026Trial
- Remimazolam attenuates myocardial ischemia/reperfusion injury by inhibiting ferroptosis involving the AKT/SLC7A11/GPX4 axis.International journal of molecular medicine · 2026Article
- Remimazolam alleviates hippocampal neuronal injury in an in vitro Alzheimer's disease model by promoting PINK1/Parkin-mediated mitophagy.European journal of medical research · 2025Article
- Mollugin attenuates oxygen-glucose deprivation/reperfusion-induced brain microvascular endothelial cell death and permeability through activation of BDNF/TrkB-modulated Akt pathway.Journal of bioenergetics and biomembranes · 2025Article
- Antioxidative Activity of Remimazolam as a Direct Free Radical Scavenger in Comparison With Midazolam.Cureus · 2025Article
- miRNA-105 Attenuates Hypoxic-Ischemic Brain Damage in Neonatal Rats by Inhibiting Apoptosis and Necroptosis.Neurochemical research · 2025Article
- ROS-responsive dextran-benzeneboronic acid pinacol ester micelles encapsulating edaravone for the treatment and mechanism of cerebral ischemia-reperfusion injury.Metabolic brain disease · 2025Article
- Remimazolam attenuated lipopolysaccharide-induced behavioral deficits and neuronal injury via activation of the Nrf2 pathway.Scientific reports · 2025Article
- Safety of Remimazolam in Vulnerable Populations.Drug design, development and therapy · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The mechanism of remimazolam, a benzodiazepine that activates γ-aminobutyric acid a (GABAa) receptors, in cerebral ischemia/reperfusion (I/R) injury is not well understood. Therefore, we explored whether remimazolam activates protein kinase B (AKT)/glycogen synthase kinase-3β (GSK-3β)/nuclear factor erythroid 2-related factor 2 (NRF2) to attenuate brain I/R injury in transcerebral I/R-injured rats and transoxygenic glucose deprivation/reperfusion (OGD/R)-injured SY5Y cells. Material and Methods: Remimazolam was added at the beginning of cell and rat reperfusion, and the PI3K/AKT inhibitor LY294002 was added to inhibit the AKT/GSK-3β/NRF2 pathway 24 h before cellular OGD/R treatment and 30 min before rat brain I/R treatment. The viability and apoptosis rate of SY5Y cells, neurological deficit score, cerebral infarction volume and morphological changes of rat brain cells as well as the protein expression of Bax, Bcl2, Caspase 3, Cleaved-Caspase 3 and the number of TdT-mediated dUTP Nick-End Labeling (TUNEL)-positive cells in the penumbral region were detected. Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), NRF2, heme oxygenase 1 (HO-1), AKT, P-AKT, GSK-3β, P-GSK-3β protein expression, and nuclear translocation of NRF2 were measured in cell and animal assays. Results: Reduced SY5Y cell viability and increased apoptosis caused by OGD/R injury, elevated neurological deficit scores and cerebral infarct volume induced by brain I/R injury in rats, cerebral cell injury, as well as elevated Bax, Cleaved-Caspase 3, decreased Bcl2, and increased number of TUNEL-positive cells in rat brain tissue were all moderated by remimazolam. Decreased GSH-Px, SOD and Elevated MDA, ROS induced by OGD/R-injured SY5Y cells and brain I/R-injured rats were moderated by remimazolam. Meanwhile, remimazolam increased NRF2, HO-1, P-AKT, P-GSK-3β, and the nuclear accumulation of NRF2. The PI3K/AKT inhibitor LY294002 reversed the role of remimazolam in brain I/R injury. Conclusion: This study demonstrates that remimazolam activates the AKT/GSK-3β/NRF2 pathway, thereby attenuating oxidative stress and apoptosis to protect against brain I/R injury.
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