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Sevoflurane alleviates oxygen-glucose deprivation/reoxygenation-induced damage in HT22 cells by activating the Keap1/Nrf2/ARE pathway to inhibit oxidative stress.

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Title: Sevoflurane alleviates oxygen-glucose deprivation/reoxygenation-induced damage in HT22 cells by activating the Keap1/Nrf2/ARE pathway to inhibit oxidative stress.
Authors: Yan, Ke (AUTHOR), Li, Lei (AUTHOR), Ye, Siqi (AUTHOR), Xu, Qiao (AUTHOR), Ding, Li (AUTHOR)
Source: International Journal of Neuroscience. Jan2025, Vol. 135 Issue 1, p110-117. 8p.
Subjects: Nuclear factor E2 related factor, Reactive oxygen species, Glutathione peroxidase, Mitochondrial membranes, Membrane potential
Abstract: Objective: This study aimed to investigate the impact of sevoflurane on oxygen-glucose deprivation/reoxygenation-induced damage in HT22 cells and its associated mechanisms. Methods: HT22 cells were treated with sevoflurane, and an oxygen-glucose deprivation/reoxygenation injury model was established. The HT22 cells were randomly divided into the control group, oxygen-glucose deprivation/reoxygenation group, sevoflurane low-dose group, sevoflurane medium-dose group, and sevoflurane high-dose group. The proliferation of HT22 cells was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptosis rate and mitochondrial membrane potential of HT22 cells were determined by flow cytometry. Protein expression levels of B-cell lymphoma-2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein 1 (Keap1), and heme oxygenase-1 (HO-1) in HT22 cells were examined using Western blot. Reactive oxygen species (ROS) levels were measured with 2',7'-dichlorofluorescin diacetate (DCFH-DA). Malondialdehyde (MDA), glutathione peroxidase (GSH-Px) levels, and superoxide dismutase (SOD) enzyme activity in HT22 cells were determined using assay kits. Results: Compared to controls, OGD/R group had reduced cell viability, mitochondrial potential, Bcl-2, nuclear Nrf2, HO-1, GSH-Px levels, and SOD enzyme activity (p < 0.05), with increased apoptosis, Bax, cytoplasmic Nrf2, ROS, and MDA levels. Sevoflurane groups showed opposite trends (p < 0.05). Conclusion: Sevoflurane can mitigate oxygen-glucose deprivation/reoxygenation-induced damage in HT22 cells, and its mechanism may be related to the activation of the Keap1/Nrf2/ARE pathway to inhibit oxidative stress. [ABSTRACT FROM AUTHOR]
Copyright of International Journal of Neuroscience is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Sevoflurane alleviates oxygen-glucose deprivation/reoxygenation-induced damage in HT22 cells by activating the Keap1/Nrf2/ARE pathway to inhibit oxidative stress.
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  Data: &lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Yan%2C+Ke%22&quot;&gt;Yan, Ke&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Li%2C+Lei%22&quot;&gt;Li, Lei&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Ye%2C+Siqi%22&quot;&gt;Ye, Siqi&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Xu%2C+Qiao%22&quot;&gt;Xu, Qiao&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Ding%2C+Li%22&quot;&gt;Ding, Li&lt;/searchLink&gt; (AUTHOR)
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  Data: &lt;searchLink fieldCode=&quot;JN&quot; term=&quot;%22International+Journal+of+Neuroscience%22&quot;&gt;International Journal of Neuroscience&lt;/searchLink&gt;. Jan2025, Vol. 135 Issue 1, p110-117. 8p.
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  Data: &lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Nuclear+factor+E2+related+factor%22&quot;&gt;Nuclear factor E2 related factor&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Reactive+oxygen+species%22&quot;&gt;Reactive oxygen species&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Glutathione+peroxidase%22&quot;&gt;Glutathione peroxidase&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Mitochondrial+membranes%22&quot;&gt;Mitochondrial membranes&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Membrane+potential%22&quot;&gt;Membrane potential&lt;/searchLink&gt;
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  Label: Abstract
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  Data: Objective: This study aimed to investigate the impact of sevoflurane on oxygen-glucose deprivation/reoxygenation-induced damage in HT22 cells and its associated mechanisms. Methods: HT22 cells were treated with sevoflurane, and an oxygen-glucose deprivation/reoxygenation injury model was established. The HT22 cells were randomly divided into the control group, oxygen-glucose deprivation/reoxygenation group, sevoflurane low-dose group, sevoflurane medium-dose group, and sevoflurane high-dose group. The proliferation of HT22 cells was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptosis rate and mitochondrial membrane potential of HT22 cells were determined by flow cytometry. Protein expression levels of B-cell lymphoma-2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), nuclear factor erythroid 2-related factor 2 (Nrf2), Kelch-like ECH-associated protein 1 (Keap1), and heme oxygenase-1 (HO-1) in HT22 cells were examined using Western blot. Reactive oxygen species (ROS) levels were measured with 2&#39;,7&#39;-dichlorofluorescin diacetate (DCFH-DA). Malondialdehyde (MDA), glutathione peroxidase (GSH-Px) levels, and superoxide dismutase (SOD) enzyme activity in HT22 cells were determined using assay kits. Results: Compared to controls, OGD/R group had reduced cell viability, mitochondrial potential, Bcl-2, nuclear Nrf2, HO-1, GSH-Px levels, and SOD enzyme activity (p &lt; 0.05), with increased apoptosis, Bax, cytoplasmic Nrf2, ROS, and MDA levels. Sevoflurane groups showed opposite trends (p &lt; 0.05). Conclusion: Sevoflurane can mitigate oxygen-glucose deprivation/reoxygenation-induced damage in HT22 cells, and its mechanism may be related to the activation of the Keap1/Nrf2/ARE pathway to inhibit oxidative stress. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: &lt;i&gt;Copyright of International Journal of Neuroscience is the property of Taylor &amp; Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder&#39;s express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.&lt;/i&gt; (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1080/00207454.2023.2286916
    Languages:
      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 8
        StartPage: 110
    Subjects:
      – SubjectFull: Nuclear factor E2 related factor
        Type: general
      – SubjectFull: Reactive oxygen species
        Type: general
      – SubjectFull: Glutathione peroxidase
        Type: general
      – SubjectFull: Mitochondrial membranes
        Type: general
      – SubjectFull: Membrane potential
        Type: general
    Titles:
      – TitleFull: Sevoflurane alleviates oxygen-glucose deprivation/reoxygenation-induced damage in HT22 cells by activating the Keap1/Nrf2/ARE pathway to inhibit oxidative stress.
        Type: main
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          Name:
            NameFull: Yan, Ke
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            NameFull: Li, Lei
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            NameFull: Ye, Siqi
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            NameFull: Xu, Qiao
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            NameFull: Ding, Li
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            – D: 01
              M: 01
              Text: Jan2025
              Type: published
              Y: 2025
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              Value: 135
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            – TitleFull: International Journal of Neuroscience
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