Toxicology and applied pharmacology
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Toxicol. Appl. Pharmacol. · Jul 2009
Comparative StudyDiclofenac enhances proinflammatory cytokine-induced nitric oxide production through NF-kappaB signaling in cultured astrocytes.
Recently, the number of reports of encephalitis/encephalopathy associated with influenza virus has increased. In addition, the use of a non-steroidal anti-inflammatory drug, diclofenac sodium (DCF), is associated with a significant increase in the mortality rate of influenza-associated encephalopathy. Activated astrocytes are a source of nitric oxide (NO), which is largely produced by inducible NO synthase (iNOS) in response to proinflammatory cytokines. ⋯ Addition of DCF further augments NO production. This effect is mediated via NF-kappaB signaling and leads to cell damage. The enhancement of DCF on NO production may explain the significant increase in the mortality rate of influenza-associated encephalopathy in patients treated with DCF.