ArticleExperimental and therapeutic medicine2021
Sevoflurane alleviates oxygen-glucose deprivation/reoxygenation-induced injury in HT22 cells through regulation of the PI3K/AKT/GSK3β signaling pathway.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Elucidating multifaceted targets of Marein in cerebral ischemia-reperfusion injury.Frontiers in chemistry · 2025Article
- Hypericin alleviates cerebral ischemia/reperfusion injury by modulating endoplasmic reticulum stress.Frontiers in pharmacology · 2025Article
- Role of phosphorylated Y1252, Y1336 and Y1472 on NR2B subunits in hypoxia tolerance of neuronal cell in vitro.Experimental brain research · 2024Article
- Absorbed Bioactive Compounds Replicate Guanxin II-Induced Endothelium-Associated in/ex vivo Vasodilation.Chinese journal of integrative medicine · 2024Article
- Sevoflurane protects against cerebral ischemia/reperfusion injury via microrna-30c-5p modulating homeodomain-interacting protein kinase 1.Bioengineered · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
Sevoflurane (Sev), a volatile anesthetic, has been reported to exhibit beneficial effects on different ischemia/reperfusion (I/R)-injured organs. However, the neuroprotective effect of Sev on cerebral I/R injury is poorly understood. In the present study, the effects of Sev on HT22 cells exposed to oxygen-glucose deprivation/reperfusion (OGD/R) injury are investigated. The present study demonstrated that OGD/R suppressed the cell viability and increased lactate dehydrogenase (LDH) release from the cells, and these effects were attenuated by Sev treatment. The results also demonstrated that Sev alleviated OGD/R-induced cell apoptosis via flow cytometry and caspase-3 activity determination. Biochemical analysis results revealed that Sev significantly protected against OGD/R-induced oxidative stress by reducing ROS generation and improving antioxidant defense markers. Western blot analysis demonstrated that Sev reactivated the PI3K/AKT/glycogen synthase kinase-3β (GSK3β) signaling pathway, which was inhibited by OGD/R. In addition, wortmannin, a selective PI3K inhibitor was used to investigate the underlying pathways. Notably, the neuroprotective effect of Sev on apoptosis and reactive oxygen species production was found to be suppressed by wortmannin. Collectively, these results demonstrated that Sev may protect neuronal cells against OGD/R-induced injury through the activation of the PI3K/AKT/GSK3β signaling pathway. The findings from the present study provide a novel insight into understanding the neuroprotective effect of Sev on cerebral I/R injury.
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