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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: Astrocyte-derived SerpinA3N promotes neuroinflammation and epileptic seizures by activating the NF-κB signaling pathway in mice with temporal lobe epilepsy

Fig. 3

SerpinA3N overexpression aggravates KA-induced neuroinflammation and increases the number of hippocampal astrocytes and microglia in vivo. A The mRNA levels of TNF-α, Il-1β, Il-18, Il-6, and NF-κB in the hippocampus of SerpinA3N-overexpressing mice at 35 d post-SE, as determined by qPCR (n = 4). Normalized to the NC + veh level. GAPDH served as the internal control. B, C Western blotting and densitometric quantitative analysis of TNF-α, IL-1β and IL-18 in the hippocampal CA3 area of SerpinA3N-overexpressing mice at 35 d post-SE (n = 4). Normalized to the NC + veh level. GAPDH served as the internal control. D, E Representative fluorescence micrographs of GFAP and IBA1 expression in the hippocampus CA3 of SerpinA3N-overexpressing mice with or without KA treatment for 35 days. Scale bar = 50 μm. F, G The panels show the cell counts of cells positive for GFAP and IBA1 (n = 4). All data are shown as the mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. SE: status epilepticus; NC: empty AAV vectors; Veh: vehicle; KA: kainic acid; OE: AAV vectors containing overexpression serpina3n

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