ArticleDrug design, development and therapy2018
Sevoflurane post-conditioning attenuates traumatic brain injury-induced neuronal apoptosis by promoting autophagy via the PI3K/AKT signaling pathway.
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 77 citations in OpenAlex.
- Eerdun Wurile, a Mongolian medicine, alleviates neuronal damage and improves neurological dysfunction after cerebral hemorrhage by activating the PI3K/AKT signaling pathway.Chinese medicine · 2026Article
- A closed-head, rotational traumatic brain injury model demonstrates deficits in righting reflex, neurological function, and auditory brainstem responses in rats.Brain injury · 2026Article
- CircRNA circ_0004058 Modulates Early Brain Injury in Subarachnoid Hemorrhage Through miR-221-3p and VE1 Activation Pathway.Translational stroke research · 2025Article
- Antisecretory Factor 16 (AF16): A Promising Avenue for the Treatment of Traumatic Brain Injury-An In Vitro Model Approach.Journal of molecular neuroscience : MN · 2024Article
- Adiponectin deficiency is a critical factor contributing to cognitive dysfunction in obese mice after sevoflurane exposure.Molecular medicine (Cambridge, Mass.) · 2024Article
- Quinoa ameliorates polycystic ovary syndrome via regulating gut microbiota through PI3K/AKT/mTOR pathway and autophagy.Nutrition & metabolism · 2024Article
- Microglia-induced neuroinflammation in hippocampal neurogenesis following traumatic brain injury.Heliyon · 2024Review
- Article
- Based on Bioinformatics to Explore the Mechanism of "Tangzhiqing" Decoction Alleviating Type 2 Diabetes-associated Cognitive Dysfunction in Mice by Regulating Hippocampal Neuron Apoptosis and Autophagy.Combinatorial chemistry & high throughput screening · 2024Article
- Transcriptomic and bioinformatics analysis of the mechanism by which erythropoietin promotes recovery from traumatic brain injury in mice.Neural regeneration research · 2024Article
- GATA6 Inhibits Neuronal Autophagy and Ferroptosis in Cerebral ischemia-reperfusion Injury Through a miR-193b/ATG7 axis-dependent Mechanism.Neurochemical research · 2023Article
- Inhibiting phosphatase and actin regulator 1 expression is neuroprotective in the context of traumatic brain injury.Neural regeneration research · 2023Article
- Sevoflurane Preconditioning Alleviates Posttraumatic Stress Disorder-Induced Apoptosis in the Hippocampus via the EZH2-Regulated Akt/mTOR Axis and Improves Synaptic Plasticity.Journal of molecular neuroscience : MN · 2023Article
- Roles of microRNA-124 in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2023Review
- Models of traumatic brain injury-highlights and drawbacks.Frontiers in neurology · 2023Review
- Article
- miRNA-384-3p alleviates sevoflurane-induced nerve injury by inhibiting Aak1 kinase in neonatal rats.Brain and behavior · 2022Article
- Macamide B Pretreatment Attenuates Neonatal Hypoxic-Ischemic Brain Damage of Mice Induced Apoptosis and Regulates Autophagy via the PI3K/AKT Signaling Pathway.Molecular neurobiology · 2022Article
- The neuroprotective mechanism of sevoflurane in rats with traumatic brain injury via FGF2.Journal of neuroinflammation · 2022Article
- New insights into the interplay between autophagy and oxidative and endoplasmic reticulum stress in neuronal cell death and survival.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSevoflurane post-conditioning exerts nerve-protective effects through inhibiting caspase-dependent neuronal apoptosis after a traumatic brain injury (TBI). Autophagy that is induced by the endoplasmic reticulum stress plays an important role in the secondary neurological dysfunction after a TBI. However, the relationship between autophagy and caspase-dependent apoptosis as well as the underlying nerve protection mechanism that occurs with sevoflurane post-conditioning following a TBI remains unclear.
methodsThe Feeney TBI model was used to induce brain injury in rats. Evaluation of the modified neurological severity scores, measurement of brain water content, Nissl staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay were used to determine the neuroprotective effects of the sevoflurane post-conditioning. Both immunofluorescence and Western blot analyses were used to detect the expression of autophagy-related proteins microtubule-associated protein 1 light chain 3-II and Beclin-1, pro-apoptotic factors, as well as the activation of the phosphatidylinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway within the lesioned cortex.
resultsAutophagy and neuronal apoptosis were activated in the lesioned cortex following the TBI. Sevoflurane post-conditioning enhanced early autophagy, suppressed neuronal apoptosis, and alleviated brain edema, which improved nerve function after a TBI (all
conclusionNeuronal apoptosis and the activation of autophagy were involved in the secondary neurological injury following a TBI. Sevoflurane post-conditioning weakened the TBI-induced neuronal apoptosis by regulating autophagy via PI3K/AKT signaling.
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