Diethylcarbamazine (DEC) interferes with cyclooxygenase and lipoxygenase pathways, reducing the production of thromboxane, prostacyclin, prostaglandin and leukotrienes. Recent studies using different experimental models of inflammation have indicated that DEC, in addition to inhibiting cyclooxygenase and lipoxygenase pathways, also inhibits nuclear transcription factor kappa B (NF-κB) activation, which is a key regulator of proinflammatory genes such as TNF-α, IL-1β, inducible nitric oxide synthase (iNOS) and even cyclooxygenase 2 (COX-2). The aim of the present study is to provide a comprehensive summary of DEC, including a description of filaricidal action, inhibition of synthesis and secretory pathways, immunomodulatory activity, and specific inhibition of lipoxygenase and cyclooxygenase pathways.
Keywords: Cyclooxygenase; Diethylcarbamazine; Lipoxygenase; NF-κB.
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