ArticleBioengineered2022
Propofol induces the apoptosis of neural stem cells via microRNA-9-5p / chemokine CXC receptor 4 signaling pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- High-Dose Propofol Induces Cytotoxicity by Elevating Intracellular CaDrug design, development and therapy · 2026Article
- Induction of M1 polarization in BV2 cells by propofol intervention promotes perioperative neurocognitive disorders through the NGF/CREB signaling pathway: an experimental research.International journal of surgery (London, England) · 2025Article
- Exploring the correlation between Drp1 protein and the neurotoxicity of propofol.Frontiers in neuroscience · 2025Review
- Research progress of propofol in alleviating cerebral ischemia/reperfusion injury.Pharmacological reports : PR · 2024Review
- Dexmedetomidine Protects Cortical Neurons from Propofol-Induced Apoptosis via Activation of Akt-IKK-NF-κB Signaling Pathway by αApplied biochemistry and biotechnology · 2024Article
- Neuraxial Anesthesia for Combined Left Nephrectomy and Left Hemicolectomy in a One-Lung Patient.Cureus · 2024Article
- Determination of the embryotoxic effects of propofol injected into eggs on the cerebellum and spinal cord using histologic methods: an animal study.Turkish journal of medical sciences · 2024Article
- Role of ferroptosis in hypoxic preconditioning to reduce propofol neurotoxicity.Frontiers in pharmacology · 2023Article
- Recent progress on the role of non-coding RNA in postoperative cognitive dysfunction.Frontiers in cellular neuroscience · 2022Review
- Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies suggested that propofol, one of the most widely used anesthetics, may cause neurotoxicity in the developing brain, leading to cognitive deficits in adults. However, the underlying mechanisms remain unclear. In this study, we aimed to evaluate the mechanisms of propofol neurotoxicity in the neural stem cells (NSCs). The mRNA and protein expression levels of microRNA-9-5p (miR-9-5p) and chemokine CXC receptor 4 (CXCR4) were determined by quantitative reverse transcription-polymerase chain reaction and Western blotting analyses. Cell viability and apoptosis were evaluated using the cell counting kit-8 and Hoechst staining kits. The levels of apoptosis-related proteins B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, and caspase-3 were detected by Western blotting analysis. These results confirmed that propofol activated cell apoptosis in a dose-dependent manner. A significant increase in the miR-9-5p and CXCR4 expression was observed in the propofol-treated cells. The overexpression of miR-9-5p induced apoptosis in NSCs, accompanied by elevated apoptosis-related protein activity. Furthermore, mitigated CXCR4 expression reduced propofol-induced cell apoptosis. We conclude that propofol induces cell death in NSCs, and overexpression of miR-9-5p/CXCR4 contributes to propofol-induced cell apoptosis, which might be a target for developing novel strategies to treat propofol neurotoxicity.
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