Fig. 7From: 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 periodTSA reversed the effects of MS on the activation of NF-κB signaling and neuroinflammatory responses to sevoflurane in the hippocampal tissues in adult MS rats. a TSA pretreatment prevented the enhancement effect of MS on the levels of nuclear NF-κB p65 protein 12 h after anesthesia. b–d TSA pretreatment suppressed the increase in hippocampal TNF-α, IL-1β, and IL-6 levels 12 h after anesthesia in adult MS rats. e The fluorescence intensities of GFAP and p-NF-κB p65 in the TSA group rats were obviously lower than those in the DMSO group rats. 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. f The changes in the fluorescence intensities 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 DMSO. Error bars represent the means ± SD (n = 6). Statistical analyses were performed with Student’s two-sample t testBack to article page