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Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis

  • Authors:
    • Zhi‑Bin Zhou
    • Xiao‑Yu Yang
    • Ying Tang
    • Xue Zhou
    • Li‑Hua Zhou
    • Xia Feng
  • View Affiliations / Copyright

    Affiliations: Department of Anesthesiology, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China, Department of Anatomy, Zhong Shan Medical College, Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China
    Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 721-727
    |
    Published online on: May 24, 2016
       https://doi.org/10.3892/mmr.2016.5336
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Abstract

Sevoflurane is generally considered a pro-apoptotic agent in the neonatal brain. However, recent studies have suggested that low levels of sevoflurane anesthesia may be neuroprotective and have a memory enhancing effect. The present study aimed to investigate whether sevoflurane exerts a neuroprotective effect at subclinical concentrations, with regard to oxidative state. In the current study, postnatal day 7 (P7) Sprague‑Dawley rats were continuously exposed to 0.3, 1.3, or 2.3% sevoflurane for 6 h. ELISA was used to quantify the levels of superoxide dismutase, glutathione peroxidase (GSH‑px) and malondialdehyde (MDA) in the plasma and the hippocampus. Terminal deoxynucleotidyl-transferase dUTP nick-end labeling staining was used to observe hippocampal neuronal apoptosis. Altered object exploration tests for recognition memory were employed to investigate long‑term behavioral effects at postnatal day 28. The results demonstrated that a single 6 h exposure to a subclinical concentration (1.3%) of sevoflurane at P7 reduces MDA and GPH‑px production in rats. Sevoflurane induced hippocampal apoptosis in a dose‑dependent manner and altered recognition memory testing indicated no differences among the groups. Although early exposure to a subclinical concentration of sevoflurane reduced oxidative stress, it did not prevent the process of sevoflurane-induced hippocampal apoptosis. These changes did not affect subsequent recognition memory in juvenile rats.
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Copy and paste a formatted citation
Spandidos Publications style
Zhou ZB, Yang XY, Tang Y, Zhou X, Zhou LH and Feng X: Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis. Mol Med Rep 14: 721-727, 2016.
APA
Zhou, Z., Yang, X., Tang, Y., Zhou, X., Zhou, L., & Feng, X. (2016). Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis. Molecular Medicine Reports, 14, 721-727. https://doi.org/10.3892/mmr.2016.5336
MLA
Zhou, Z., Yang, X., Tang, Y., Zhou, X., Zhou, L., Feng, X."Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis". Molecular Medicine Reports 14.1 (2016): 721-727.
Chicago
Zhou, Z., Yang, X., Tang, Y., Zhou, X., Zhou, L., Feng, X."Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis". Molecular Medicine Reports 14, no. 1 (2016): 721-727. https://doi.org/10.3892/mmr.2016.5336
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou ZB, Yang XY, Tang Y, Zhou X, Zhou LH and Feng X: Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis. Mol Med Rep 14: 721-727, 2016.
APA
Zhou, Z., Yang, X., Tang, Y., Zhou, X., Zhou, L., & Feng, X. (2016). Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis. Molecular Medicine Reports, 14, 721-727. https://doi.org/10.3892/mmr.2016.5336
MLA
Zhou, Z., Yang, X., Tang, Y., Zhou, X., Zhou, L., Feng, X."Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis". Molecular Medicine Reports 14.1 (2016): 721-727.
Chicago
Zhou, Z., Yang, X., Tang, Y., Zhou, X., Zhou, L., Feng, X."Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis". Molecular Medicine Reports 14, no. 1 (2016): 721-727. https://doi.org/10.3892/mmr.2016.5336
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