ArticleJournal of anesthesia2018
Pink1 attenuates propofol-induced apoptosis and oxidative stress in developing neurons.
Article in Journal of anesthesia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Multi-omics analysis reveals sevoflurane exacerbates cognitive impairment in diabetic mice by disrupting lipid metabolism.Scientific reports · 2026Article
- Mitophagy in perioperative neurocognitive disorder: mechanisms and therapeutic strategies.European journal of medical research · 2025Review
- EMC1 Is Required for the Sarcoplasmic Reticulum and Mitochondrial Functions in theBiomolecules · 2024Article
- Propofol Suppresses LPS-induced BBB Damage by Regulating miR-130a-5p/ZO-1 Axis.Molecular biotechnology · 2024Article
- Toll-Like Receptor 4 Deficiency Ameliorates Propofol-Induced Impairments of Cognitive Function and Synaptic Plasticity in Young Mice.Molecular neurobiology · 2024Article
- Screening of potential biomarkers in propofol-induced neurotoxicity via bioinformatics prediction and experimental verification.American journal of translational research · 2024Article
- The effects of general anesthetics on mitochondrial structure and function in the developing brain.Frontiers in neurology · 2023Review
- Propofol induces the apoptosis of neural stem cells via microRNA-9-5p / chemokine CXC receptor 4 signaling pathway.Bioengineered · 2022Article
- Esketamine improves propofol-induced brain injury and cognitive impairment in rats.Translational neuroscience · 2022Article
- Propofol protects hippocampal neurons in sleep-deprived rats by inhibiting mitophagy and autophagy.Annals of translational medicine · 2021Article
- The Role of Pink1-Mediated Mitochondrial Pathway in Propofol-Induced Developmental Neurotoxicity.Neurochemical research · 2021Article
- Downregulation of HOTAIR reduces neuronal pyroptosis by targeting miR-455-3p/NLRP1 axis in propofol-treated neurons in vitro.Neurochemical research · 2021Article
- Article
- PINK1 alleviates thermal hypersensitivity in a paclitaxel-induced Drosophila model of peripheral neuropathy.PloS one · 2020Article
- Overexpression of phosphoprotein enriched in astrocytes 15 reverses the damage induced by propofol in hippocampal neurons.Molecular medicine reports · 2019Article
- Potential role of the cAMP/PKA/CREB signalling pathway in hypoxic preconditioning and effect on propofol‑induced neurotoxicity in the hippocampus of neonatal rats.Molecular medicine reports · 2019Article
- [Exposure to propofol down-regulates myelin basic protein expression in zebrafish embryos: its neurotoxicity on oligodendrocytes and the molecular mechanisms].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe underlying mechanisms of propofol-induced neurotoxicity in developing neurons are still not completely understood. We examined the role of PTEN-induced kinase 1 (Pink1), an antioxidant protein, in propofol-induced apoptosis in developing neurons. MATERIALS AND
methodsPrimary hippocampal neurons isolated from neonatal Sprague-Dawley rats were exposed to propofol 20 μM for 2, 4, 6 and 12 h. Subsequently, neurons underwent overexpression and knockdown of Pink1, followed by propofol exposure (20 μM, 6 h). Neuron apoptosis was detected by terminal transferase deoxyuridine triphosphate-biotin nick-end labeling (TUNEL). Reactive oxygen species (ROS) production in neurons was detected by using a 2,7-dichlorodihydro-fluorescein diacetate probe and target protein or mRNA levels were analyzed by Western blotting or real-time polymerase chain reaction.
resultsPropofol treatment time-dependently increased the number of TUNEL-positive neurons and the expression levels of cleaved caspase-3 and B-cell lymphoma 2 (BcL-2) associated X protein, but decreased expression levels of BcL-2. Furthermore, propofol treatment time-dependently reduced the expression levels of Pink1 mRNA and protein. ROS production and the markers of oxidative stress, 2,4-dinitrophenol and 4-hydroxynonenal, were increased by propofol treatment. However, these propofol-induced changes were significantly restored by Pink1 overexpression.
conclusionsPink1 plays an important role in neuronal apoptosis induced by propofol. Our results may provide some new insights in propofol-induced neurotoxicity in developing neurons.
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