Table 1 Clinical studies reporting COX-2 involvement in epilepsy
From: Cyclooxygenase-2 (COX-2) inhibitors: future therapeutic strategies for epilepsy management
Reference | Study type | Tissue | Cells | Study subjects | Reference |
|---|---|---|---|---|---|
Desjardins et al. [99] | Expression | Hippocampus | Astrocytes and neurons | 5 sclerotic and 2 non-sclerotic DRTLE | Induction of astrocytic COX-2 in patients with HS suggesting its implication in the pathogenesis of HS in epilepsy |
Holtman et al. [98] | Expression | Hippocampus | Astrocytes and neurons | 6 sclerotic and 4 non-sclerotic DRTLE and 5 controls | Higher astrocytic and neuronal COX-2 in patients with HS compared to non-HS and controls |
Das et al. [19] | Expression | Hippocampus | Astrocytes and neurons | 6 sclerotic DRTLE and 3 sudden-death controls | Increased COX-2 in patients suggesting its crucial role in TLE pathogenesis |
Hung et al. [101] | Genetic | Whole blood | White blood cells | 35 children with febrile seizures and 31 controls | A single SNP, rs689466, localized at 5′-1192 of the PTGS2 gene was significantly association with febrile seizures |
Weidner et al. [100] | Expression | Hippocampus | Microglia, astrocytes and neurons | 16 sclerotic and 17 non-sclerotic DRTLE | Higher microglial and neuronal COX-2 expression than astrocytic COX-2 No difference in COX-2 levels among sclerotic and non-sclerotic samples |