ArticlePloS one2017
Sevoflurane protects rat brain endothelial barrier structure and function after hypoxia-reoxygenation injury.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 62 citations in OpenAlex.
- The NLRP3 Inflammasome: A Central Mediator in Sevoflurane-Induced Neurotoxicity and A Potential Target for Neuroprotection.Molecular neurobiology · 2026Review
- Aberrant expression and regulatory role of histone deacetylase 9 in vascular endothelial cell injury in intracranial aneurysm.Biomolecules & biomedicine · 2024Article
- The duration-dependent and sex-specific effects of neonatal sevoflurane exposure on cognitive function in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- Review
- Effects of sevoflurane on lung epithelial permeability in experimental models of acute respiratory distress syndrome.Journal of translational medicine · 2023Article
- Article
- Prolonged anesthesia induces neuroinflammation and complement-mediated microglial synaptic elimination involved in neurocognitive dysfunction and anxiety-like behaviors.BMC medicine · 2023Article
- Neuropeptide Y: An Update on the Mechanism Underlying Chronic Intermittent Hypoxia-Induced Endothelial Dysfunction.Frontiers in physiology · 2021Review
- Acorus tatarinowii Schott extract reduces cerebral edema caused by ischemia-reperfusion injury in rats: involvement in regulation of astrocytic NKCC1/AQP4 and JNK/iNOS-mediated signaling.BMC complementary medicine and therapies · 2020Article
- DHA Attenuates Hypoxia/Reoxygenation Injury by Activating SSeCKS in Human Cerebrovascular Pericytes.Neurochemical research · 2020Article
- Sub-Toxic Human Amylin Fragment Concentrations Promote the Survival and Proliferation of SH-SY5Y Cells via the Release of VEGF and HspB5 from Endothelial RBE4 Cells.International journal of molecular sciences · 2018Article
- The effect of pre- and after-treatment of sevoflurane on central ischemia tolerance and the underlying mechanisms.Journal of dental anesthesia and pain medicine · 2018Review
- The protective effects of sevoflurane on subarachnoid hemorrhage.Medical gas researchReview
- Recent advances in the neuroprotective effects of medical gases.Medical gas researchReview
- Protective effects of sevoflurane in cerebral ischemia reperfusion injury: a narrative review.Medical gas researchReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAfter cerebral injury blood-brain barrier disruption significantly impairs brain homeostasis. Volatile anesthetics have been shown to be protective in ischemia-reperfusion injury scenarios. Their impact on brain endothelial cells after hypoxia-reoxygenation (H/R) has not yet been studied in detail.
methodsRat brain endothelial cells (RBE4) were exposed to severe hypoxia and reoxygenated in air in the presence or absence of sevoflurane. Changes in dextran permeability and architecture of the cellular junctional proteins ZO-1 and β-catenin were measured. To determine necrosis and apoptosis rate DNA content, LDH release and caspase activity were quantified. The role of vascular endothelial growth factor (VEGF) as an inflammatory mediator increasing vascular permeability was assessed. At the same time, it was evaluated if sevoflurane effects are mediated through VEGF. Results were analyzed by unpaired t-tests or one way-analysis of variance followed by Bonferroni's correction.
resultsH/R led to a 172% increase in permeability (p<0.001), cell swelling and qualitatively but not quantitatively modified expression of ZO-1, β-catenin and F-actin. In the presence of sevoflurane during reoxygenation, barrier function improved by 96% (p = 0.042) in parallel to a decrease of the cell size and less re-arranged junction proteins and F-actin. Sevoflurane-induced improvement of the barrier function could not be explained on the level of necrosis or apoptosis as they remained unchanged independent of the presence or absence of the volatile anesthetic. Increased expression of VEGF after H/R was attenuated by sevoflurane by 34% (p = 0.004). Barrier protection provided by sevoflurane was similar to the application of a blocking VEGF-antibody. Furthermore, the protective effect of sevoflurane was abolished in the presence of recombinant VEGF.
conclusionsIn H/R-induced rat brain endothelial cell injury sevoflurane maintains endothelial barrier function through downregulation of VEGF, which is a key player not only in mediating injury, but also with regard to the protective effect of sevoflurane.
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