Dehydroevodiamine HCl is an alkaloid isolated from E. rutaecarpa and possesses anti-inflammatory, antiarrhythmic, hypotensive, and anti-amnesic biological activities.
Dehydroevodiamine (DHE) Hydrochloride (HCl) is an alkaloid isolated from E. rutaecarpa and possesses anti-inflammatory, antiarrhythmic, hypotensive, and anti-amnesic biological activities. DHE administration had an excellent therapeutic impact on the AIA (adjuvant-induced arthritis) rat model, substantially relieving joint swelling, inhibiting synovial pannus hyperplasia, and decreasing joint scores[2]. DHE suppressed the viability of HCT116, CT26, SW480, and LoVo cells. DHE treatment led to G2/M arrest via a reduction of cyclin B1/CDK1 and caspase-dependent apoptosis. It also induced autophagy by regulating LC3-II and beclin-1 expression. Additionally, migration and invasion of CRC cells were decreased by DHE through regulation of the expression of EMT markers. Oral administration of DHE could inhibit the lung metastasis of CT26 cells in an in vivo model[3]. A single (20 mg/kg p.o.) and repeated (10 mg/kg p.o.) administrations of DHED (dehydroevodiamine.HCl) could significantly reverse the latency time shortened by scopolamine (1 mg/kg i.p.) to control level. The cognitive deficits caused by EC lesion and middle cerebral artery occlusion were improved significantly by repeated administrations of DHED (6.25 mg/kg i.p.) after EC lesion or ischemic insult once a day for 7 days in the passive avoidance test[4].
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