Open Access

Apoptosis inhibition is involved in improvement of sevoflurane‑induced cognitive impairment following normobaric hyperoxia preconditioning in aged rats

  • Authors:
    • Ying Wang
    • Chun-Ping Yin
    • Yan-Lei Tai
    • Zi-Jun Zhao
    • Zhi-Yong Hou
    • Qiu-Jun Wang
  • View Affiliations

  • Published online on: January 11, 2021     https://doi.org/10.3892/etm.2021.9636
  • Article Number: 203
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Sevoflurane, a commonly used anesthetic agent has been confirmed to induce cognitive impairment in aged rats. Normobaric hyperoxia preconditioning has been demonstrated to induce neuroprotection in rats. The present study aimed to determine whether normobaric hyperoxia preconditioning could ameliorate cognitive deficit induced by sevoflurane and the possible mechanism by which it may exert its effect. A total of 66, 20‑month‑old male Sprague‑Dawley rats were randomly divided into 3 groups (n=22 each): Rats in the control (C) and sevoflurane anesthesia (S) groups received no normobaric hyperoxia preconditioning before sevoflurane exposure, rats in the normobaric hyperoxia pretreatment (HO) group received normobaric hyperoxia preconditioning before sevoflurane exposure (95% oxygen for 4 continuous h daily for 6 consecutive days). The anesthesia rats (S and HO groups), were exposed to 2.5% sevoflurane for 5 h, while the sham anesthesia rats (C group) were exposed to no sevoflurane. The neurobehavioral assessment was performed using a Morris water maze test, the expressions of the apoptosis proteins were determined using western blot analysis, and the apoptosis rate and cytosolic calcium concentration were measured by flow cytometry. Normobaric hyperoxia preconditioning improved prolonged escape latency and raised the number of platform crossings induced by sevoflurane in the Morris water maze test, increased the level of bcl‑2 protein, and decreased the level of bax and active caspase‑3 protein, the apoptosis rate and cytosolic calcium concentration in the hippocampus 24 h after sevoflurane exposure. The findings of the present study may imply that normobaric hyperoxia preconditioning attenuates sevoflurane‑induced spatial learning and memory impairment, and this effect may be partly related to apoptosis inhibition in the hippocampus. In conclusion, normobaric hyperoxia preconditioning may be a promising strategy against sevoflurane‑induced cognitive impairment by inhibiting the hippocampal neuron apoptosis.
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March-2021
Volume 21 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Wang Y, Yin C, Tai Y, Zhao Z, Hou Z and Wang Q: Apoptosis inhibition is involved in improvement of sevoflurane‑induced cognitive impairment following normobaric hyperoxia preconditioning in aged rats. Exp Ther Med 21: 203, 2021.
APA
Wang, Y., Yin, C., Tai, Y., Zhao, Z., Hou, Z., & Wang, Q. (2021). Apoptosis inhibition is involved in improvement of sevoflurane‑induced cognitive impairment following normobaric hyperoxia preconditioning in aged rats. Experimental and Therapeutic Medicine, 21, 203. https://doi.org/10.3892/etm.2021.9636
MLA
Wang, Y., Yin, C., Tai, Y., Zhao, Z., Hou, Z., Wang, Q."Apoptosis inhibition is involved in improvement of sevoflurane‑induced cognitive impairment following normobaric hyperoxia preconditioning in aged rats". Experimental and Therapeutic Medicine 21.3 (2021): 203.
Chicago
Wang, Y., Yin, C., Tai, Y., Zhao, Z., Hou, Z., Wang, Q."Apoptosis inhibition is involved in improvement of sevoflurane‑induced cognitive impairment following normobaric hyperoxia preconditioning in aged rats". Experimental and Therapeutic Medicine 21, no. 3 (2021): 203. https://doi.org/10.3892/etm.2021.9636