Planta Med 2007; 73 - P_584
DOI: 10.1055/s-2007-987364

Anti-dementia effect of Aralia cordata: in vitro and in vivo

SO Cho 1, JY Ban 1, KS Song 2, K Bae 3, YH Seong 1
  • 1College of Veterinary Medicine and Research Institute of Herbal Medicine, Chungbuk National University, Cheongju, Chungbuk, 361–763, Republic of Korea
  • 2College of Agriculture and Life-Sciences, Kyungpook National University, Daegu 702–701, Republic of Korea
  • 3College of Pharmacy, Chungnam National University, Taejon 305–764, Republic of Korea

Alzheimer's disease (AD) is characterized by neuronal loss and extracellular senile plaque, whose major constituent is amyloid β protein (Aβ), a 39–43 amino acid peptide derived from amyloid precursor protein [1]. Aralia cordata Thunb. (Araliaceae) (AC) is a medicinal plant distributed in Korea, China and Japan. In a previous report, we demonstrated that the aerial part of AC contains diterpenes, triterpenes, saponins, sterols and cerebroside and its inhibitory activity against COX-1 and COX-2 [2]. The neuroprotective and antidementia effects of a 70% ethanol extract of aerial part of AC were examined using primarily cultured neurons and experimental animals in the present study. It was demonstrated that AC (1–10µg/ml) inhibited Aβ (25–35)-induced neuronal apoptotic death, generation of reactive oxygen species and elevation of [Ca2+]i in primarily cultured rat cortical neurons. Memory loss by Aβ (25–35) (8 nmol, i.c.v.), examined in passive avoidance test, was recovered by chronic treatment of AC (50 and 100mg/kg, p.o., 8 days) in ICR mice. In the same system, brain and blood acetylcholinesterase activity induced by Aβ (25–35) was inhibited by AC supporting the in vivo results. In Morris water maze test [3], scopolamine (1mg/kg, i.p.)-induced amnesia was prevented by AC administration (100 and 200mg/kg, p.o., 5 days) in C57BL6 mice. Data were expressed as mean±SEM and statistical significance was assessed by one-way analysis of variance (ANOVA) with subsequent Tukey's tests. From these results, it is concluded that the protection against Aβ (25–35)-induced neurotoxicity and dementia by AC may help to explain its inhibitory action on the progression of AD.

Acknowledgements: BioGreen 21 Program (2006), Rural Development Administration, Republic of Korea.

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