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Original Research

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Chrysotoxine attenuates sevoflurane-induced neurotoxicity in vitro via regulating PI3K/AKT/GSK pathway

  • Jin Qiu1
  • Yi Zhang2
  • Mian Xie1

1Department of Anesthesiology, Chongqing Hospital of TCM, 400021 Chongqing City, Chongqing, China

2Department of Anesthesiology, The Second Affiliated Hospital of Zunyi Medical University, 563000 Zunyi City, Guizhou Province, China

DOI: 10.22514/sv.2021.107 Vol.17,Issue 4,July 2021 pp.185-191

Submitted: 27 May 2021 Accepted: 15 June 2021

Published: 08 July 2021

*Corresponding Author(s): Mian Xie E-mail: mianx7644@163.com

Abstract

Objective: The aim of this study is to investigate the neuroprotective effect of chrysotoxine (CTX) on sevoflurane-treated nerve cells and uncover the potential regulation mechanism.

Methods: Nerve cells treated with sevoflurane and CTX were subjected to MTT and apoptotic detection. Cell apoptosis and oxidative stress were detected by flow cytometry (FCM) and ELISA assays. In addition, immunoblot assay was performed to study the signaling pathway affected by CTX treatment.

Results: CTX treatment promoted the cell viability and suppressed the apoptosis of sevoflurane-treated SH-SY5Y cells. In addition, CTX inhibited the sevoflurane-induced oxidative stress response and inflammatory response in nerve cells. Mechanically, CTX ameliorated neurotoxicity through activating the PI3K/AKT/GSK signaling pathway.

Conclusion: Therefore, CTX can serve as a promising drug target for treating anesthetics-induced neurotoxicity.


Keywords

Sevoflurane; Chrysotoxine (CTX); Neurotoxicity; Apoptosis; PI3K/AKT/GSK pathway


Cite and Share

Jin Qiu,Yi Zhang,Mian Xie. Chrysotoxine attenuates sevoflurane-induced neurotoxicity in vitro via regulating PI3K/AKT/GSK pathway. Signa Vitae. 2021. 17(4);185-191.

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