Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway

Background: Sevoflurane (Sev) is an inhalational anesthetic for surgical procedures where it can trigger cognitive dysfunction and neuronal apoptosis. Gyosaponin (GpS) was studied for its effects on brain morphology and cognitive behaviors in Sev-anesthetized rats. Methods: Male Sprague-Dawley rats...

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Autores: Lin, Lijuan, Zhu, Chenhui, Yan, Bing, Yu, Pinxian, Yang, Liu, Huang, Wei, Chen, Junren
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2025
País:Brasil
Institución:Universidade de São Paulo (USP)
Repositorio:Clinics
Idioma:inglés
OAI Identifier:oai:revistas.usp.br:article/238063
Acceso en línea:https://revistas.usp.br/clinics/article/view/238063
Access Level:acceso abierto
Palabra clave:Gyosaponin
Sevoflurane
Cognitive Dysfunction
Neuronal Cell Apoptosis
PI3K/AKT/mTOR Pathway
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spelling Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathwayGyosaponinSevofluraneCognitive DysfunctionNeuronal Cell ApoptosisPI3K/AKT/mTOR PathwayBackground: Sevoflurane (Sev) is an inhalational anesthetic for surgical procedures where it can trigger cognitive dysfunction and neuronal apoptosis. Gyosaponin (GpS) was studied for its effects on brain morphology and cognitive behaviors in Sev-anesthetized rats. Methods: Male Sprague-Dawley rats were induced by 3% Sev anesthesia, and 25 mg/kg and 100 mg/kg GpS were injected into the rats by tail vein. The in vitro model of Sev anesthesia was constructed by treating primary rat hippocampal neurons with 4.1% Sev in the presence of GpS (5, 10, and 20 μM). The neuroprotective effects of GpS against Sev-induced cognitive deficits in rats were evaluated using the open field and Morris water maze tests. The apoptosis of hippocampal neurons was observed using HE staining and TUNEL assay. Apoptosis-related proteins and proteins related to the PI3K/Akt/mTOR pathway were determined via Western blot. Also, proinflammatory factors were measured via ELISA. Results: GpS diminished the Sev-triggered apoptosis in neurons and Cleaved caspase-3, BAX, TNF-α, IL-6, lessened oxidative stress damage, and stimulated the PI3K/Akt/mTOR pathway. GpS therapy markedly enhanced learning and memory abilities in rats suffering from Sev-related cognitive impairments. Conclusion: GpS ameliorates Sev-induced neurotoxicity and cognitive dysfunction by modulating the PI3K/Akt/mTOR pathway and alleviating neuronal apoptosis and oxidative stress.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2025-01-27info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://revistas.usp.br/clinics/article/view/23806310.1016/Clinics; Vol. 80 (2025); 100560Clinics; v. 80 (2025); 100560Clinics; Vol. 80 (2025); 1005601980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://revistas.usp.br/clinics/article/view/238063/214931Copyright (c) 2025 Clinicsinfo:eu-repo/semantics/openAccessLin, LijuanZhu, ChenhuiYan, BingYu, PinxianYang, LiuHuang, WeiChen, Junren2025-09-12T13:44:54Zoai:revistas.usp.br:article/238063Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2025-09-12T13:44:54Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway
title Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway
spellingShingle Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway
Lin, Lijuan
Gyosaponin
Sevoflurane
Cognitive Dysfunction
Neuronal Cell Apoptosis
PI3K/AKT/mTOR Pathway
title_short Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway
title_full Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway
title_fullStr Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway
title_full_unstemmed Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway
title_sort Gyosaponin ameliorates sevoflurane anesthesia-induced cognitive dysfunction and neuronal apoptosis in rats through modulation of the PI3K/AKT/mTOR pathway
dc.creator.none.fl_str_mv Lin, Lijuan
Zhu, Chenhui
Yan, Bing
Yu, Pinxian
Yang, Liu
Huang, Wei
Chen, Junren
author Lin, Lijuan
author_facet Lin, Lijuan
Zhu, Chenhui
Yan, Bing
Yu, Pinxian
Yang, Liu
Huang, Wei
Chen, Junren
author_role author
author2 Zhu, Chenhui
Yan, Bing
Yu, Pinxian
Yang, Liu
Huang, Wei
Chen, Junren
author2_role author
author
author
author
author
author
dc.subject.por.fl_str_mv Gyosaponin
Sevoflurane
Cognitive Dysfunction
Neuronal Cell Apoptosis
PI3K/AKT/mTOR Pathway
topic Gyosaponin
Sevoflurane
Cognitive Dysfunction
Neuronal Cell Apoptosis
PI3K/AKT/mTOR Pathway
description Background: Sevoflurane (Sev) is an inhalational anesthetic for surgical procedures where it can trigger cognitive dysfunction and neuronal apoptosis. Gyosaponin (GpS) was studied for its effects on brain morphology and cognitive behaviors in Sev-anesthetized rats. Methods: Male Sprague-Dawley rats were induced by 3% Sev anesthesia, and 25 mg/kg and 100 mg/kg GpS were injected into the rats by tail vein. The in vitro model of Sev anesthesia was constructed by treating primary rat hippocampal neurons with 4.1% Sev in the presence of GpS (5, 10, and 20 μM). The neuroprotective effects of GpS against Sev-induced cognitive deficits in rats were evaluated using the open field and Morris water maze tests. The apoptosis of hippocampal neurons was observed using HE staining and TUNEL assay. Apoptosis-related proteins and proteins related to the PI3K/Akt/mTOR pathway were determined via Western blot. Also, proinflammatory factors were measured via ELISA. Results: GpS diminished the Sev-triggered apoptosis in neurons and Cleaved caspase-3, BAX, TNF-α, IL-6, lessened oxidative stress damage, and stimulated the PI3K/Akt/mTOR pathway. GpS therapy markedly enhanced learning and memory abilities in rats suffering from Sev-related cognitive impairments. Conclusion: GpS ameliorates Sev-induced neurotoxicity and cognitive dysfunction by modulating the PI3K/Akt/mTOR pathway and alleviating neuronal apoptosis and oxidative stress.
publishDate 2025
dc.date.none.fl_str_mv 2025-01-27
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://revistas.usp.br/clinics/article/view/238063
10.1016/
url https://revistas.usp.br/clinics/article/view/238063
identifier_str_mv 10.1016/
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://revistas.usp.br/clinics/article/view/238063/214931
dc.rights.driver.fl_str_mv Copyright (c) 2025 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2025 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 80 (2025); 100560
Clinics; v. 80 (2025); 100560
Clinics; Vol. 80 (2025); 100560
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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score 15.300724

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