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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: 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 period

Fig. 7

TSA 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 test

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