Fig. 3From: Enhanced neuroinflammation mediated by DNA methylation of the glucocorticoid receptor triggers cognitive dysfunction after sevoflurane anesthesia in adult rats subjected to maternal separation during the neonatal periodMS enhanced the activation of astrocytes and the astroglial NF-κB signaling pathway induced by 3% sevoflurane anesthesia for 2 h in the hippocampus. a Sevoflurane anesthesia increased the fluorescence intensity of glial fibrillary acidic protein (GFAP) and phosphorylated nuclear factor-kappa B (p-NF-κB p65) in the CA1 area of the hippocampus at 12 h after anesthesia in both the sevoflurane group and MS + sevoflurane group, and the fluorescence intensity of GFAP and p-NF-κB p65 in the MS + sevoflurane group was obviously higher than that in the sevoflurane group. Double immunofluorescence staining showed that p-NF-κB p65 (green) mainly co-localized (merged) with GFAP-positive reactive astrocytes (red) in the CA1 area of the hippocampus. b The changes in the fluorescence intensity of GFAP and p-NF-κB p65 in the DG area of the hippocampus were similar to those in the CA1 area of the hippocampus. * P < 0.05, ** P < 0.01 versus control; ## P < 0.01 versus MS; ++ P < 0.01 MS + sevoflurane versus sevoflurane. Error bars represent the means ± SD (n = 6). Statistical analyses were performed by one-way ANOVA followed by Student–Newman–Keuls post hoc test. CA1 cornu ammonis 1, DG dentate gyrus; bar = 100 μmBack to article page