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. 2017 May 15;127(6):2118–2132. doi: 10.1172/JCI92001

Figure 4. Early prediction of epilepsy development by monitoring blood HMGB1 level in lithium+pilocarpine SE rats.

Figure 4

(A) Longitudinal analysis of total HMGB1 and acetylated, reduced, and disulfide isoform levels in blood at representative time points of disease development (see key in A). Blood was drawn at 23 days (epileptogenic phase prodromal to epilepsy onset), 73 days (encompassing the time of disease onset in 70% of rats), and 7.5 months (chronic epilepsy). Data represent mean ± SEM; n = 7 sham; n = 5 epileptic (Epi); n = 5 nonepileptic (Nonepi) rats. Dot plots are shown in Supplemental Figure 10. **P < 0.01 (refers to both isoforms in each bar); P < 0.05, acetylated HMGB1 in epileptic versus sham, Kruskal-Wallis test. Total HMGB1, acetylated and disulfide isoform levels in the chronic phase (Epi) are significantly different versus corresponding levels in prodromal phase (P < 0.01, repeated measures 1-way ANOVA). (B) Representative immunohistochemical pictures of CA1 stratum radiatum depicting HMGB1 staining in control (sham, n = 7) and in SE rats with (Epi, n = 5 out of 12) or without (Nonepi, n = 5) spontaneous seizures. Rats are the same as reported in A. Brains were harvested 7.5 months after SE. Arrows, nuclear staining of HMGB1 in sham and nonepileptic rats; arrowheads, cytoplasmic HMGB1 staining in glia in epileptic rats. Scale bar: 15 μm.