ArticleJournal of anesthesia2016
Isoflurane postconditioning induces concentration- and timing-dependent neuroprotection partly mediated by the GluR2 AMPA receptor in neonatal rats after brain hypoxia-ischemia.
Article in Journal of anesthesia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Preconditioning and Posttreatment Strategies in Neonatal Hypoxic-Ischemic Encephalopathy: Recent Advances and Clinical Challenges.Molecular neurobiology · 2025Review
- Post-Treatment Sevoflurane Protects Against Hypoxic-Ischemic Brain Injury in Neonatal Rats by Downregulating Histone Methyltransferase G9a and Upregulating Nuclear Factor Erythroid 2-Related Factor 2 (NRF2).Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Nutraceuticals in the Prevention of Neonatal Hypoxia-Ischemia: A Comprehensive Review of their Neuroprotective Properties, Mechanisms of Action and Future Directions.International journal of molecular sciences · 2021Review
- Isoflurane reduces septic neuron injury by HO‑1‑mediated abatement of inflammation and apoptosis.Molecular medicine reports · 2021Article
- An appropriate level of autophagy reduces emulsified isoflurane-induced apoptosis in fetal neural stem cells.Neural regeneration research · 2020Article
- Clinical Implications of Epigenetic Dysregulation in Perinatal Hypoxic-Ischemic Brain Damage.Frontiers in neurology · 2020Review
- Evaluation of Altered Glutamatergic Activity in a Piglet Model of Hypoxic-Ischemic Brain Damage UsingDisease markers · 2020Article
- The role of PI3K-mediated AMPA receptor changes in post-conditioning of propofol in brain protection.BMC neuroscience · 2019Article
- P2X7 Receptors Mediate CO-Induced Alterations in Gene Expression in Cultured Cortical Astrocytes-Transcriptomic Study.Molecular neurobiology · 2019Article
- Sevoflurane post-conditioning alleviates neonatal rat hypoxic-ischemic cerebral injury via Ezh2-regulated autophagy.Drug design, development and therapy · 2019Article
- Positive and negative conditioning in the neonatal brain.Conditioning medicine · 2018Article
- Ischemic Conditioning and neonatal hypoxic ischemic encephalopathy: a literature review.Conditioning medicine · 2017Article
- Neuroprotection provided by isoflurane pre-conditioning and post-conditioning.Medical gas researchReview
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9 authors.
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Abstract
backgroundIt has been demonstrated that preconditioning with 1.5 % isoflurane reduces hypoxia/ischemia (HI)-induced brain loss/injury in neonatal rats. Ca(2+) influx mediated by α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors (AMPARs) is involved in HI-induced neuronal death. Here, we investigated the effective concentrations and time windows for neuroprotection by isoflurane postconditioning in neonatal rats after brain HI and determined whether GluR2-containing AMPARs mediate this neuroprotection.
methodsSeven-day-old Sprague-Dawley (SD) rats were randomly divided into eight groups (n = 40 in each). The rats underwent left common carotid arterial ligation (brain HI) or sham surgery, followed by exposure to 8 % oxygen for 2 h at 37 °C in a thermoregulated environment. Post-conditioning with 1, 1.5, or 2 % isoflurane for 30 min was performed immediately after brain HI. Others were post-treated with 1.5 % isoflurane for 30 min at 3, 6, and 12 h after brain HI. The weight ratio, neuronal density ratio in the ventral posteromedial thalamic nucleus, and retrosplenial granular cortex of left to right cerebral hemispheres at 7 days after brain HI were evaluated in all groups. Cerebral hemispheres were harvested for Western-blot analysis of GluR2 on the cellular membranes 24 h after HI or sham surgery in neonatal rats from the sham group, the HI group, and the HI + immediate exposure to the 1.5 % isoflurane group. In another experiment, the function of learning and memory were assessed in adolescence (4 weeks) using Morris water maze.
resultsCompared with the control (sham) group, brain HI decreased the weight ratio and the neuronal density ratio in the ventral posteromedial thalamic nucleus and the retrosplenial granular cortex of the left to right cerebral hemispheres (p < 0.05). These effects of brain HI were reduced by postconditioning with 1.5 or 2 % isoflurane for 30 min within 6 h of HI, which coincided with the results of Morris water maze. GluR2 protein expression on cellular membranes was reduced after HI compared with sham surgery group (p < 0.05); this down-regulation was attenuated by isoflurane postconditioning.
conclusionsPostconditioning with 1.5 and 2 % isoflurane affords neuroprotection in neonatal rats. The time window for isoflurane postconditioning to be effective against neonatal HI-induced brain injury was 0-6 h after HI. This protection may be mediated by GluR2-containing AMPARs.
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