Dehydroevodiamine is an alkaloid isolated from E. rutaecarpa and possesses anti-inflammatory, antiarrhythmic, hypotensive, and anti-amnesic biological activities.
Dehydroevodiamine (DHED) is a major bioactive quinazoline alkaloid isolated from Evodiae Fructus, and has an antiarrhythmic effect in guinea-pig ventricular myocytes[3]. 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[4]. Similarly to the cholinesterase inhibitor, physostigmine (0.03--0.3 mg/kg, i.p.), dehydroevodiamine (0.75--12.0 mg/kg, i.p.) administered 30 min before the training trial, immediately after the training trial, and 30 min before the retention test significantly improved scopolamine- and beta-amyloid peptide-(25--35)-induced amnesia[5]. DHED (10 mg/kg, p.o.) and Donepezil (1 mg/kg, p.o.) ameliorated the spatial memory impairment in the scopolamine-induced amnestic rats[6]. DHED could suppress the overactivation of GSK-3 (glycogen synthase kinase-3) and improve tau hyperphosphorylation and spatial memory deficit of the rats[7]. DHED (Pre-incubation of the brain slices with DHED) can attenuate CA(calyculin A)-induced tau hyperphosphorylation at multiple AD-related sites in metabolically active rat brain slices[8].
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