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 inflamm...

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Bibliographic Details
Published in:	Neuroscience research Vol. 38; no. 2; pp. 209 - 212
Main Authors:	Matoth, Israel, Pinto, Florance, Sicsic, Camille, Brenner, Talma
Format:	Journal Article
Language:	English
Published:	Ireland Elsevier Ireland Ltd 01-10-2000
Subjects:	Animals Anticonvulsants - pharmacology Carbamazepine Carbamazepine - pharmacology Cells, Cultured Central nervous system inflammation Dinoprostone - antagonists & inhibitors Dose-Response Relationship, Drug Glial cells Inflammation Mediators - antagonists & inhibitors Inflammation Mediators - metabolism Lipopolysaccharides - pharmacology Neuroglia - drug effects Neuroglia - metabolism Nitric oxide Nitric Oxide - antagonists & inhibitors Phospholipase A 2 Phospholipases A - antagonists & inhibitors Phospholipases A - secretion Prostaglandins Rats Prostaglandins Phospholipase A 2 Glial cells Central nervous system inflammation Nitric oxide Carbamazepine
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Summary:	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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0168-0102 1872-8111
DOI:	10.1016/S0168-0102(00)00127-9