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Phytomedicine. 2012 Dec 15;20(1):84-8. doi: 10.1016/j.phymed.2012.09.005. Epub 2012 Oct 15.

Lancemaside A isolated from Codonopsis lanceolata and its metabolite echinocystic acid ameliorate scopolamine-induced memory and learning deficits in mice.

Author information

1
Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, 1 Hoegi, Dongdaemun-gu, Seoul 130-701, Republic of Korea.

Abstract

The rhizome of Codonopsis lanceolata (family Campanulaceae), which contains lancemaside A as a main constituent, has been used as herbal medicine to treat inflammation, insomnia, and hypomnesia. Lancemaside A and echinocystic acid, which is its metabolite by intestinal microflora, potently inhibited acetylcholinesterase activity in a dose-dependent manner, with IC₅₀ value 13.6 μM and 12.2 μM, respectively. Its inhibitory potency is comparable with that of donepezil (IC₅₀=10.9 μM). Lancemaside A and echinocystic acid significantly reversed scopolamine-induced memory and learning deficits on passive avoidance task. Lancemaside A orally administered 5h before treatment with scopolamine reversed scopolamine-induced memory and learning deficits more potently than one orally administered 1h before. Echinocystic acid more potently reversed it than lancemaside A. Lancemaside A and echinocystic acid significantly reversed scopolamine-induced memory and learning deficits on the Y-maze and Morris water maze tasks. Lancemaside A and echinocystic acid also increased the expression of brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element binding protein (p-CREB). Based on these findings, orally administered lancemaside A may be metabolized to echinocystic acid, which may be absorbed into the blood and ameliorate memory and learning deficits by inhibiting AChE activity and inducing BDNF and p-CREB expressions.

PMID:
23079229
DOI:
10.1016/j.phymed.2012.09.005
[Indexed for MEDLINE]

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