ArticleTranslational neuroscience2022
Esketamine improves propofol-induced brain injury and cognitive impairment in rats.
Article in Translational neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 18 citations in OpenAlex.
- Network pharmacology and experimental verification to explore the therapeutic mechanism of esketamine in postoperative cognitive dysfunction.Molecular and cellular biochemistry · 2026Article
- Esketamine at a Clinical Dose Attenuates Cerebral Ischemia/Reperfusion Injury by Inhibiting AKT Signaling Pathway to Facilitate Microglia M2 Polarization and Autophagy.Drug design, development and therapy · 2025Article
- Identification of Key Genes in Esketamine's Therapeutic Effects on Perioperative Neurocognitive Disorders via Transcriptome Sequencing.Drug design, development and therapy · 2025Article
- Safety and efficacy evaluation of low-dose of esketamine combined with propofol for painless gastroscopy: a single-center, randomized, double-blind, parallel controlled clinical trial.Frontiers in medicine · 2025Article
- Associations of BDNF/BDNF-AS SNPs with Depression, Schizophrenia, and Bipolar Disorder.Journal of personalized medicine · 2023Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As an intravenous anesthetic, propofol has been indicated to induce neurotoxicity in both animal and human brains. It is of great significance to better understand the potential mechanism of propofol-induced neurotoxicity to eliminate the side effects of propofol. Esketamine is a sedative that has been proven to have an antidepressant effect. However, its effect on propofol-induced neurotoxicity and the underlying mechanism remain unclear. Herein, we investigated the role of esketamine in propofol-induced brain injury. A rat model of propofol-induced brain injury was established with or without the treatment of esketamine. The results demonstrated that propofol-induced impairment in spatial learning and memory of rats and promoted oxidative stress, neuronal injury and apoptosis in rat hippocampal tissues. The effects caused by propofol were attenuated by esketamine. Esketamine activated the mature brain-derived neurotrophic factor/tropomyosin receptor kinase B/phosphatidylinositide 3-kinase (mBDNF/TrkB/PI3K) signaling pathway in propofol-administrated rats. Moreover, knocking down BDNF partially reversed esketamine-mediated activation of the mBDNF/TrkB/PI3K signaling pathway and inhibition of neuronal apoptosis in propofol-induced rats. Overall, esketamine mitigates propofol-induced cognitive dysfunction and brain injury in rats by activating mBDNF/TrkB/PI3K signaling.
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