Planta Med 2008; 74 - PA202
DOI: 10.1055/s-0028-1084200

Inhibition of monoamine oxidase and acetylcholinesterase by Rhodiola rosea L

D van Diermen 1, A Marston 1, J Bravo 2, M Reist 2, PA Carrupt 2, K Hostettmann 1
  • 1Laboratory of Pharmacognosy and Phytochemistry
  • 2LCT-Pharmacochemistry, School of Pharmaceutical Sciences, University of Geneva, University of Lausanne, Quai Ernest-Ansermet 30, CH-1211 Geneva 4, Switzerland

Rhodiola rosea L. (Crassulaceae), the most investigated species of the genus Rhodiola, grows at elevated altitude in the Arctic and in mountainous regions throughout Europe and Asia, where it is also known as „golden root“ or „arctic root“. The roots have been used for centuries in the traditional medicine of Asia, Scandinavia and Eastern Europe to stimulate the nervous system, treat depression, enhance physical and mental performance, improve resistance to high altitude sickness and to treat fatigue and psychological stress [1].

Although clinical studies have provided evidence that administration of R. rosea extract elicits antidepressant activity [2,3], the mechanism of action of R. rosea in the treatment of nervous system disorders still remains unclear.

The present study aims at explaining the influence of a root extract of R. rosea on mood disorders by studying its effect on the metabolism of monoamine neurotransmitters. To this end, three extracts, dichloromethane, methanol and water, were tested against MAO-A and MAO-B in a microtitre plate assay and against acetylcholinesterase (AChE) on TLC. The first extract showed AChE inhibitory activity and the latter two extracts presented MAO inhibitory activity. Therefore a bio-guided fractionation of the extracts was undertaken in order to identify the active compounds. Nine compounds were isolated and identified by means of spectroscopic and chemical methods, including 1D and 2D NMR experiments and MS analysis. The MAO and AChE inhibitory activities are reported here, together with the main components of each active extract that account for the demonstrated inhibitory activities.

References: 1. Khanum, F. et al. (2005) Comp Rev Food Sci Food safety 4:55–62.

2. Kurkin, V. et al. (2006) Pharm Chem J 40:614–619.

3. Perfumi, M., Mattioli, L. (2007) Phytother Res 21:37–43.