Fig. 1
NADPH oxidase deletion reduced the increased pentylenetetrazole (PTZ)-induced seizure susceptibility following lipopolysaccharide (LPS) stimulation. a The experiment protocol is schematized. Wild-type (WT), gp91phox−/−, and p47phox−/− mice were injected intraperitoneally (i.p.) with 4 mg/kg lipopolysaccharide (LPS). Plasma samples were collected 1 h later for TNFα quantification and some mice were sacrificed 24 h later for the preparation of brain sections and transcript assays. Two days later, seizure susceptibility to 60 mg/kg PTZ (i.p.) was evaluated (n = 6 or 7 mice per genotype). b The latency to initial seizure onset (clonic with/without tonic convulsion) after PTZ administration. Data are presented as mean ± SEM. Bonferroni post hoc test vs. LPS-treated WT group; *p < 0.05, **p < 0.01. c Seizure susceptibility of gp91phox−/−, and p47phox−/− and WT mice scored once every 5 min over the 2-h period following PTZ injection. Two-way repeated measures ANOVA revealed that the main effect for LPS-treated WT, gp91phox−/−, and p47phox−/−groups yielded an F ratio of F(2, 432) = 34.12, p < 0.0001, Bonferroni post-test analysis further revealed significant difference between the WT group and gp91phox−/− (F(1,288) = 42.63; p < 0.0001) and between WT and p47phox−/− (F(1,288) = 54.86; p < 0.0001), but no difference between p47phox−/− and gp91phox−/− groups ((F(1,288) = 1.16; p = 0.282). d The total duration (min) of seizure behavior ≥ stage 4. Data are presented as mean ± SEM. Bonferroni post hoc test vs. vehicle-treated or LPS-treated WT group; **p < 0.01, ***p < 0.001