Status Epilepticus Induces Vasogenic Edema via Tumor Necrosis Factor-α/ Endothelin-1-Mediated Two Different Pathways
Figure 1
The roles of TNF-α in SE-induced vasogenic edema in the PC.
(A) The extracellular TNF-α concentration after SE (mean ± s.d., n = 5): *P < 0.05 versus the basal level; paired Student’s t-test. (B and C) Quantification of western blots for TNF-α protein expression and p65-Thr435 NFκB phosphorylation 12 h after SE (means ± s.e.m., n = 5, respectively); *P < 0.05 by Student’s t-test. (D–I) Immunofluorescence data for TNFp75R, p65-Thr435 NFκB phosphorylation and SMI-71 12 h after SE. (J–K) Effects of TNFp55R and SN50 on p65-Thr435 NF-κB phosphorylation and SMI-71 immunoreactivity. (L–M) Quantification of the fluorescence intensities of SMI-71 expression and p65-Thr435 NFκB phosphorylation 12 h after SE (means ± s.e.m., n = 5, respectively); *P < 0.05 versus non-SE animals; #P < 0.05 versus vehicle-treated animals; one-way analysis of variance (ANOVA) followed by Tukey’s test. (N–Q) Quantification of vasogenic edema attenuation by sTNFp55R and SN50 3 days after SE (means ± s.e.m., n = 5, respectively); *P < 0.05 versus vehicle treated animals by one-way ANOVA followed by Tukey’s test. Scale bars: D–K, 25 μm; O-Q, 400 μm.