Inhibitory effect of carbamazepine on inflammatory mediators produced by stimulated glial cells

Exposure of rat glial cells to lipopolysaccharide (LPS) induces the production of nitric oxide (NO) and prostaglandin E 2 (PGE 2), the inflammatory mediators implicated in the pathogenesis of seizures and epilepsy. To determine the effect of the anticonvulsant drug carbamazepine (CBZ) on the inflammatory process, LPS-stimulated rat primary glial cultures were exposed to this agent. Dose-dependent inhibition of NO and PGE 2 production was observed of up to 77 and 88%, respectively. Furthermore, a prominent (94%) decline in the secretory isoform of phospholipase A 2 (sPLA 2) activity was found in response to CBZ and could contribute to the inhibition of PGE 2 production. Cumulatively, our findings point to the anti-inflammatory effect of CBZ on non-neuronal cells, which might, in part, contribute to its anticonvulsive effect.