Abstract

BackgroundValerian is commonly used for the treatment of insomnia and anxiety. Valerian extracts allosterically modulate GABA-A receptors and induced an anxiolytic activity. This activity is closely related to valerenic acid. In the present experiments it was investigated whether acetoxy valerenic acid may interfere with the anxiolytic action of valerenic acid.MethodsSituational anxiety was measured using male CD-1 mice in the elevated plus maze test after oral administration of the test substances. In addition the body core temperature was measured. For the 3H-GABA binding assay dissected tissue from frontal cortex of male RjHan:WI rats were used. Statistical evaluation was performed by means of the non-parametric Kruskal-Wallies H-test, followed by the two-tailed Mann–Whitney U-test.ResultsAdding of acetoxy valerenic acid abolished the anxiolytic action of valerenic acid. There was no effect on body core temperature. Moreover, the valerian extract did not show any affinity to benzodiazepine binding sites.ConclusionThe determining compound for the observed anxiolytic effect of the valerian extract is its content of valerenic acid.

Highlights

  • Valerian is commonly used for the treatment of insomnia and anxiety

  • Elevated plus maze For the animal groups treated with 0.5 mg valerenic acid (VA) /kg with added acetoxy valerenic acid (AVA) a significant effect was found (Χ2 4, 87 = 24.37, p < 0.001)

  • In conclusion, the VA content of Valerian extract (VE) seems to be an important factor for the observed anxiolytic activity

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Summary

Introduction

Valerian extracts allosterically modulate GABA-A receptors and induced an anxiolytic activity. This activity is closely related to valerenic acid. In-vitro experiments demonstrated that valerian extracts allosterically modulate GABA-A receptors [1,2,3], an action related to valerenic acid [4,5]. These results were confirmed with in-vivo rodent studies [1,2]. Valerian extract (VE) was fractionated and the fractions were tested with respect to their ability to allosterically modulate GABA-A receptors. The fractions with high VA and low AVA demonstrated the most pronounced allosteric action [5]

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