ArticleApplied biochemistry and biotechnology2024
Dexmedetomidine Protects Cortical Neurons from Propofol-Induced Apoptosis via Activation of Akt-IKK-NF-κB Signaling Pathway by α
Article in Applied biochemistry and biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Targeting neuroimmune interactions: the therapeutic potential of kaempferol in immune-related central nervous system disorders.Frontiers in immunology · 2026Review
- Dexmedetomidine administration may be beneficial in relation to ventilator-associated pneumonia.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextPropofol can induce neuroapoptosis. It has been reported that dexmedetomidine (DEX) has a protective effect on propofol-induced neuroapoptosis, but the specific mechanism needs to be further explored to provide a theoretical basis for their combined use.
objectiveWe aimed to explore the neuroprotective effect of DEX on primary cortical neurons treated by propofol and to elucidate the underlying mechanistic pathways.
methodsCortical neurons were isolated from fetal rats and treated with propofol. MTT assays were performed to detect cell viability, α-tubulin immunofluorescent assays were conducted to observe cell abnormalities, and c-caspase3 immunofluorescent assays and flow cytometry were performed to examine cell apoptosis. Further, neurons were cotreated with propofol and DEX to study DEX's neuroprotective effects on propofol-caused neuronal injuries. Finally, the α
resultsPropofol decreased cell viability in a dose-dependent manner, triggered apoptosis, caused morphological abnormalities and down-regulated the phosphorylation levels of Akt, IKK, NF-κB and IκB in cortical neurons. DEX ameliorated the decrease of cell viability, alleviated neuronal apoptosis and promoted the downregulated expression levels of p-Akt, IKK, NF-κB, and IκB proteins which had been induced by propofol treatment. Western blot findings following the transfection of α
conclusionDEX protected neurons against propofol-induced apoptosis via activation of the Akt-IKK-NF-κB signal pathway through α
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