ArticleNeurotoxicity research2016
The Fas Ligand/Fas Death Receptor Pathways Contribute to Propofol-Induced Apoptosis and Neuroinflammation in the Brain of Neonatal Rats.
Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- The Fas-FasL system: from apoptosis regulator to therapeutic target in autoimmunity, cancer, and transplantation.Immunologic research · 2026Review
- Intermittent Propofol Exposure Induces Neurodevelopmental Alterations in Human Brain Organoids.Cellular and molecular neurobiology · 2026Article
- From neurotoxicity to neuroprotection: Rethinking GABACell biology and toxicology · 2025Review
- Recent Advances in the Mechanisms of Postoperative Neurocognitive Dysfunction: A Narrative Review.Biomedicines · 2025Review
- Advances in research on propofol-induced postoperative cognitive dysfunction via Piezo channels.Frontiers in molecular neuroscience · 2025Review
- Damage-associated molecular patterns as a mechanism of sevoflurane-induced neuroinflammation in neonatal rodents.Korean journal of anesthesiology · 2024Article
- Mdivi-1 alleviates ferroptosis induced by hypoxia combined with propofol in HT22 cells by inhibiting excessive mitophagy.Molecular biology reports · 2024Article
- General anesthetic agents induce neurotoxicity through oligodendrocytes in the developing brain.Zoological research · 2024Review
- Effect of General Anesthetic Agents on Microglia.Aging and disease · 2024Review
- Screening of potential biomarkers in propofol-induced neurotoxicity via bioinformatics prediction and experimental verification.American journal of translational research · 2024Article
- P2X7 receptor: A receptor closely linked with sepsis-associated encephalopathy.Open life sciences · 2024Review
- Dual roles of anesthetics in postoperative cognitive dysfunction: Regulation of microglial activation through inflammatory signaling pathways.Frontiers in immunology · 2023Review
- Epidural Anesthesia versus General Anesthesia for Total Knee Arthroplasty: Influences on Perioperative Cognitive Function and Deep Vein Thrombosis.Computational and mathematical methods in medicine · 2022Article
- Effect of operative trauma and multiple propofol anesthesia on neurodevelopment and cognitive function in developmental rats.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021Article
- RTA-408 protects against propofol-induced cognitive impairment in neonatal mice via the activation of Nrf2 and the inhibition of NF-κB p65 nuclear translocation.Brain and behavior · 2021Article
- Effects of epidural block anesthesia combined with general anesthesia on inflammatory factors, cognitive function and postoperative pain in patients with lung cancer after thoracoscopic surgery.American journal of translational research · 2021Article
- Topiramate Reverses Physiological and Behavioral Alterations by Postoperative Cognitive Dysfunction in Rat Model Through Inhibiting TNF Signaling Pathway.Neuromolecular medicine · 2020Article
- Article
- Propofol directly induces caspase-1-dependent macrophage pyroptosis through the NLRP3-ASC inflammasome.Cell death & disease · 2019Article
- Article
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
A number of experimental studies have reported that exposure to common, clinically used anesthetics induce extensive neuroapoptosis and cognitive impairment when applied to young rodents, up to 2 weeks old, in phase of rapid synaptogenesis. Propofol is the most used general anesthetic in clinical practice whose mechanisms of neurotoxicity on the developing brain remains to be examined in depth. This study investigated effects of different exposures to propofol anesthesia on Fas receptor and Fas ligand expressions, which mediate proapoptotic and proinflammation signaling in the brain. Propofol (20 mg/kg) was administered to 7-day-old rats in multiple doses sufficient to maintain 2-, 4- and 6-h duration of anesthesia. Animals were sacrificed at 0, 4, 16 and 24 h after termination of anesthesia. It was found that propofol anesthesia induced Fas/FasL and downstream caspase-8 expression more prominently in the thalamus than in the cortex. Opposite, Bcl-2 and caspase-9, markers of intrinsic pathway activation, were shown to be more influenced by propofol treatment in the cortex. Further, we have established upregulation of caspase-1 and IL-1β cytokine transcription as well as subsequent activation of microglia that is potentially associated with brain inflammation. Behavioral analyses revealed that P35 and P60 animals, neonatally exposed to propofol, had significantly higher motor activity during three consecutive days of testing in the open field, though formation of the intersession habituation was not prevented. This data, together with our previous results, contributes to elucidation of complex mechanisms of propofol toxicity in developing brain.
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