ArticlePsychopharmacology2022
Sevoflurane exposure during the second trimester induces neurotoxicity in offspring rats by hyperactivation of PARP-1.
Article in Psychopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Dexmedetomidine Mitigates Sevoflurane-Induced Neurodevelopmental Effects in Paediatric Anaesthesia: A Meta-Analysis and Preclinical Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Pooled it
- Effects of the STriatal Enriched Tyrosine Phosphatase (STEP) Inhibitor TC-2153 on Hippocampal Long-Term Depression and Synaptic Transmission: Paradoxical Effect on Phosphatase Activity and Role of Adenosine.CNS neuroscience & therapeutics · 2026Article
- N-Acety-L-Cysteine Alleviates Isoflurane-Triggered Neuronal Cell Parthanatos by Suppressing Reactive Oxygen Species Accumulation Through the Induction of c-Jun N-Terminal Kinase Signaling Pathway Inhibition.Journal of biochemical and molecular toxicology · 2025Article
- Unveiling the hidden dangers: a review of non-apoptotic programmed cell death in anesthetic-induced developmental neurotoxicity.Cell biology and toxicology · 2024Review
- Multiple sevoflurane exposures during mid-trimester induce neurotoxicity in the developing brain initiated by 15LO2-Mediated ferroptosis.CNS neuroscience & therapeutics · 2023Article
- miR-671-5p Upregulation Attenuates Blood-Brain Barrier Disruption in the Ischemia Stroke Model Via the NF-кB/MMP-9 Signaling Pathway.Molecular neurobiology · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
rationaleFetal exposure to general anesthesia may cause noteworthy neurocognitive impairment, but the mechanisms are unclear.
objectivesOur study designed to explore the potential mechanism of neurotoxicity in offspring rats after sevoflurane exposure to the pregnant rats during the second trimester.
methodsPregnant rats (G14 day) were administrated with or without 3.5% sevoflurane, 40 mg/kg 3-aminobenzamide (3-AB), inhibitor of poly ADP ribose polymerase 1 (PARP-1), or 10 mg/kg TC-2153, inhibitor of striatal-enriched phosphatase 61 (STEP61). Afterwards, the effects on expression of β-tubulin (TUJ1), neurite outgrowth inhibitor A (Nogo-A), parthanatos-related and STEP61/proline-rich tyrosine kinase 2 (Pyk2) pathway-associated proteins, and reactive oxygen species (ROS) levels were examined by immunofluorescence staining, Western blot, and dihydroethidium (DHE) staining, respectively. Moreover, morphological changes in the hippocampal CA3 region and neuronal cell death were tested by glycine silver staining and TUNEL and immunofluorescence double staining, respectively. Furthermore, spatial learning and memory functions of rats on postnatal 28-33 days (PND 28-33) were evaluated by morris water maze (MWM).
resultsMid-pregnancy exposure to sevoflurane led to excessive PARP-1 activation, poly (ADP-ribose) (PAR) polymer accumulation, apoptosis-inducing factor (AIF) nuclear translocation, and Nogo-A accumulation. Besides, sevoflurane significantly inhibited neurite growth and increased cell death in the fetal rat brain. Additionally, sevoflurane activated STEP61/Pyk2 pathway and increased ROS levels. However, 3-AB or TC-2153 significantly alleviated cell death, promoted neurites growth, and improved sevoflurane-induced spatial learning and memory impairment.
conclusionThis study proposes that sevoflurane exposure during the second trimester incudes neurotoxicity in offspring rats by hyperactivation of PARP-1 via STEP61/Pyk2 pathway.
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