Fig. 1

Pharmacological inhibition of mPGES-1 diminishes SE-promoted PGE₂ in the brain. A Schematic diagram showing the timeline for experimental procedure and treatment. Mice were treated with methylscopolamine and terbutaline (2 mg/kg each, i.p.) and 30 min later by pilocarpine (280 mg/kg, i.p.) for SE induction. SE proceeded for ~ 60 min and was then interrupted by diazepam (10 mg/kg, i.p.). After recovery for 1 h, mice were randomly treated with either vehicle or compound PBCH (10 mg/kg, i.p.). Mice were treated again at 8 h and 20 h after SE onset. All animals were sacrificed 4 d after SE for neuropathological analyses. B Behavioral seizure scores were tabulated every 5 min prior to treatment with vehicle or PBCH (N = 10). C The latency to reach behavioral SE after pilocarpine administration (P = 0.2545, unpaired t test). D PGE₂ levels in the hippocampus 1 d after SE (Left) and in the cortex 4 d after SE (Right) were measured by ELISA and normalized to tissue weights (pg/mg) for comparisons by Mann–Whitney U test. Left: *P = 0.0182 for vehicle groups; P = 0.3845 for PBCH groups. Right: **P = 0.0091 for vehicle groups; P = 0.6048 for PBCH groups. E COX inhibition assay was performed to assess the inhibition of compound PBCH on COX-1 and COX-2 with indomethacin and celecoxib as reference compounds (N = 3). All compounds were tested at 10 µM, a relatively high concentration aiming to achieve their full inhibitory potential on COX enzymes, which was demonstrated by indomethacin as a non-selective COX inhibitor and celecoxib as a selective COX-2 inhibitor. Data are presented as mean + or ± SEM