ArticleFEBS open bio2020
Lithium chloride ameliorates cognition dysfunction induced by sevoflurane anesthesia in rats.
Article in FEBS open bio, 2020. 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, 8 citations in OpenAlex.
- Compromised synaptic signal from prefrontal cortex to mediodorsal thalamus in Alzheimer's disease models and its rescue by kinase inhibitors.The Journal of physiology · 2026Article
- Co-treatment Strategy Supports Neuroprotection by Intersecting p62-Keap1-NRF2 and Autophagy Signaling Pathways in the Cellular Model of Parkinson's Disease.Cellular and molecular neurobiology · 2025Article
- Cellular Components of the Blood-Brain Barrier and Their Involvement in Aging-Associated Cognitive Impairment.Aging and disease · 2024Review
- Propofol Versus Sevoflurane General Anaesthesia for Selective Impairment of Attention Networks After Gynaecological Surgery in Middle-Aged Women: A Randomised Controlled Trial.Frontiers in psychiatry · 2022Article
- Antiviral Effect of Lithium Chloride on Replication of Marek's Disease Virus in Chicken Embryonic Fibroblasts.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Postoperative cognitive dysfunction is a common complication in elderly patients after surgeries involving anesthesia, but the underlying mechanisms are poorly understood. Lithium is a conventional treatment for bipolar disorder, which exerts a neuroprotective role in various diseases by inhibiting glycogen synthase kinase-3β (GSK-3β) in the brain and spinal cord. However, it is not known whether lithium chloride (LiCl) can protect against cognitive dysfunction induced by sevoflurane (SEV) anesthesia. Here, we examined the effects of LiCl on SEV-induced cognitive dysfunction in rats and on SEV-induced neuron apoptosis. We report that anesthesia with SEV significantly impaired memory performance, induced oxidative stress and hippocampal neuron apoptosis, and stimulated GSK-3β activity. Treatment with LiCl ameliorated SEV-induced cognitive disorder in rats by inhibiting the GSK-3β/β-catenin signaling pathway. In addition, LiCl reduced hippocampal neuron apoptosis and oxidative stress induced by SEV anesthesia. These results suggest that LiCl may have potential for development into a therapeutic agent for treatment of SEV anesthesia-induced cognitive dysfunction.
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