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Dehydroevodiamine is a major bioactive quinazoline alkaloid isolated from Evodiae Fructus, has an antiarrhythmic effect in guinea-pig ventricular myocytes[1]. Dehydroevodiamine inhibits LPS-induced iNOS, COX-2, prostaglandin E2 (PGE2) and nuclear factor-kappa B (NF-κB) expression in murine macrophage cells[2].

Dehydroevodiamine (0-50 μM; 2 hours) inhibits iNOS and COX-2 expression and prevents degradation of IκB-α in LPS induced RAW 264.7 macrophages[2]. Dehydroevodiamine (0-50 μM; 2 hours) inhibits a LPS-induced increase in the iNOS and COX-2 mRNA expression[2]. Western Blot Analysis[2] Cell Line: RAW 264.7 macrophage cells

[1]. Loh SH, et al. Antiarrhythmic effects of dehydroevodiamine in isolated human myocardium and cardiomyocytes. J Ethnopharmacol. 2014 May 14;153(3):753-62. [2]. Noh EJ, et al. Inhibition of lipopolysaccharide-induced iNOS and COX-2 expression by dehydroevodiamine through suppression of NF-kappaB activation in RAW 264.7 macrophages. Life Sci. 2006 Jul 10;79(7):695-701. Epub 2006 Mar 6.

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