Open Access

Sevoflurane attenuates brain damage through inhibiting autophagy and apoptosis in cerebral ischemia‑reperfusion rats

  • Authors:
    • Cun‑Xian Shi
    • Jin Jin
    • Xue‑Qin Wang
    • Teng Song
    • Guang‑Hong Li
    • Ke‑Zhong Li
    • Jia‑Hai Ma
  • View Affiliations

  • Published online on: November 20, 2019     https://doi.org/10.3892/mmr.2019.10832
  • Pages: 123-130
  • Copyright: © Shi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study aimed to investigate the effects of sevoflurane post‑conditioning in a rat brain cerebral ischemia‑reperfusion (I/R) model and examine its possible mechanism. Rats were randomly divided into six groups: Sham control group (Sham), I/R group, sevoflurane group (Se), Toll‑like receptor‑4 (TLR4) inhibitor group (Tak‑242), nuclear factor (NF)‑κB inhibitor group (QNZ) and Sevoflurane post‑conditioning combined with TLR4‑NF‑κB signaling pathway inhibitor group (Se + Tak‑242). Morris water maze test and tetrazolium chloride staining were used to investigate the I/R injury. The nerve cell apoptosis and autophagy in cortical tissue were detected by TUNEL and transmission electron microscopy, respectively. The expression of TLR4 protein in cortical tissue was observed by immunohistochemical staining. The expression of autophagy and apoptotic associated proteins in cortical tissues and the activity of TLR4‑NF‑κB signaling pathway were assayed by western blot analysis. Sevoflurane post‑conditioning improved the learning and memory dysfunction caused by cerebral I/R injury. The cerebral infarction area, nerve cell apoptosis and formation of autophagic vacuoles were reduced after sevoflurane administration. The expression of light chain 3II/I, Beclin‑1, Bad and Cleaved‑Caspase‑3 proteins were inhibited and the expression of Bcl‑2 protein was upregulated after sevoflurane administration. Sevoflurane post‑conditioning also inhibited the TLR4 protein and NF‑κB phosphorylation, and increased inhibitor of kBα phosphorylation. The treatment effect of Tak‑242 and QNZ groups were not significantly different compared with the Se group (P>0.05), and the Se + Tak‑242 group had the best results. The present study demonstrated that sevoflurane post‑conditioning could protect middle cerebral artery occlusion‑induced brain injury rats by inhibiting autophagy and apoptosis, and that its mechanism is related to the TLR4‑NF‑κB signaling pathway.
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January-2020
Volume 21 Issue 1

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Copy and paste a formatted citation
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Spandidos Publications style
Shi CX, Jin J, Wang XQ, Song T, Li GH, Li KZ and Ma JH: Sevoflurane attenuates brain damage through inhibiting autophagy and apoptosis in cerebral ischemia‑reperfusion rats. Mol Med Rep 21: 123-130, 2020
APA
Shi, C., Jin, J., Wang, X., Song, T., Li, G., Li, K., & Ma, J. (2020). Sevoflurane attenuates brain damage through inhibiting autophagy and apoptosis in cerebral ischemia‑reperfusion rats. Molecular Medicine Reports, 21, 123-130. https://doi.org/10.3892/mmr.2019.10832
MLA
Shi, C., Jin, J., Wang, X., Song, T., Li, G., Li, K., Ma, J."Sevoflurane attenuates brain damage through inhibiting autophagy and apoptosis in cerebral ischemia‑reperfusion rats". Molecular Medicine Reports 21.1 (2020): 123-130.
Chicago
Shi, C., Jin, J., Wang, X., Song, T., Li, G., Li, K., Ma, J."Sevoflurane attenuates brain damage through inhibiting autophagy and apoptosis in cerebral ischemia‑reperfusion rats". Molecular Medicine Reports 21, no. 1 (2020): 123-130. https://doi.org/10.3892/mmr.2019.10832