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

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.