七氟烷调控S100A8/HPX/Fra-1通路抑制脊髓缺血再灌注损伤中的铁死亡OA

Objective To investigate whether sevoflurane affects the mechanisms related to fer-roptosis in spinal cord ischemia-reperfusion injury(SCIR)by influencing the functions of S100 calci-um-bindingprotein A8(S100A8),hemopexin(HPX)genes,and Fos-related antigen-1(Fra-1).Methods A total of 45 6-week-old male SD rats were randomly divided into sham operation group,model group,and sevoflurane group,with 15 rats in each group.The SCIR model was successfully replicated in the model group and the sevoflurane group.The sevoflurane group inhaled 2.4％sevoflurane 3 h before model replication,while the model group inhaled an equal volume of air.The Basso-Beattie-Bresnahan(BBB)locomotor rating scale score was evaluated 96 h after model replica-tion.HE staining was used to observe morphological changes in spinal cord tissue.TUNEL staining was employed to count the apoptotic rate.The expression levels of S100A8 mRNA,HPX mRNA,and Fra-1 mRNA were detected by qRT-PCR.The expression levels of ferroptosis markers glutathione peroxidase 4(GPX4)and solute carrier family 7 member 11(SLC7A11)were detected by Western blot.The levels of reactive oxygen species and malondialdehyde were measured using a kit method.Results Com-pared with the sham operation group,the model group showed significantly decreased BBB scores,expression levels of GPX4 and SLC7A11,and significantly increased apoptotic rate,expression lev-els of S100A8 mRNA,HPX mRNA,and Fra-1 mRNA,as well as reactive oxygen species and ma-londialdehyde levels(P＜0.05).Compared with the model group,the sevoflurane group exhibited significantly increased BBB scores,expression levels of GPX4 and SLC7A11,and significantly de-creased apoptotic rate,expression levels of S100A8 mRNA,HPX mRNA,and Fra-1 mRNA,as well as reactive oxygen species and malondialdehyde levels(P＜0.05).Conclusion Sevoflurane inhibits the process of cellular ferroptosis in SCIR through the S100A8/HPX/Fra-1 axis.