Fig 1. mRNA expression of NLRP3 and associated signalling molecules are differently regulated after SE elicited by pilocarpine or kainic acid.
(A) Schematic representation of the NLRP3 pathway: After activation of Toll-like receptor (TLR) 4 by High-Mobility-Group-Protein (HMG) B1, nuclear factor ’kappa-light-chain-enhancer’ of activated B-cells (NFKB) 2 is activated and translocates to the nucleus. Here, it enhances transcription of NOD-like receptor protein (Nlrp) 3 and Interleukins. Subsequently, NLRP3, Apoptosis-like-speck protein (ASC) and an inactive precursor of cysteine-dependent aspartate-specific Protease (CASP) 1 assemble to form the NLRP3 inflammasome. Upon activation of the inflammasome, pro-CASP1 is cleaved and activated, which then leads to cleavage of interleukin (IL) 1B and 18, as well as proinflammatory cell death. (B) Relative mRNA levels (ΔΔCt method) of inflammasomal associated genes are analysed 72 h (n ≥ 5), 10 d (n ≥ 5) and 28 d (n ≥ 6) after pilocarpine-induced status epilepticus (SE Pilo) as well as (C) 72 h (n ≥ 4), 5 d (n ≥ 5), 10 d (n ≥ 4) and 28 d (n ≥ 6) after kainic acid-induced SE in hippocampal CA1 (SE KA) compared to non-SE controls (Ctr Pilo/Ctr KA). Relative mRNA levels of NOD-like receptor protein (Nlrp) 3 and other inflammasomal associated genes such as Asc, Casp1, Tlr4, and Nfkb2 are quantified with ΔΔCt method normalized to the ubiquitously expressed (encoding proteins that are required for all cell types) housekeeping gene β-actin after SE. Data is shown as mean ± SD and analysed with 2way ANOVA followed by Sidak’s post hoc test. Asterisks indicate significant differences between groups (control vs. SE): *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Detailed statistical values are found in S2 Table.