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

Objective: The aim of this study is to investigate the neuroprotective effect chrysotoxine (CTX) on sevoflurane-treated nerve cells and uncover potential regulation mechanism. Methods: Nerve treated with sevoflurane CTX were subjected MTT apoptotic detection. Cell apoptosis oxidative stress detected by flow cytometry (FCM) ELISA assays. In addition, immunoblot assay was performed signaling pathway affected treatment. Results: treatment promoted cell viability suppressed SH-SY5Y cells. inhibited sevoflurane-induced response inflammatory in Mechanically, ameliorated neurotoxicity through activating PI3K/AKT/GSK pathway. Conclusion: Therefore, can serve as a promising drug target for treating anesthetics-induced neurotoxicity.