Evaluation of Anxiolytic Potential of Extract and Fractions of Vigna unguiculata spp dekindtiana in Mice

Anxiety disorder is mental disease that is characterised by feeling of worry or fear that interferes with daily activity. The folkloric use of Vigna unguiculata spp dekindtiana has been reported in the management of neurological diseases such as epilepsy and anxiety. Although orthodox drugs are available for this disorder, medicinal plants have been proven to have curative potentials for this disorder with minimal side effect, hence this study. The anxiolytic property of the methanol extract and fractions of Vigna unguiculata spp dekindtiana was evaluated using elevated plus maze (EPM) and hole-board models in mice. The extract and fractions were administered orally and once daily to mice of both sexes (20.6 ± 1.5 g) at 50, 100, and 200 mg/kg dose levels. The probable mechanism of anxiolytic-like activity was assessed using flumazenil, yohimbine and cyproheptadine antagonists as receptor probes. One-way ANOVA was applied for the analysis of data and significance level was determined at p < 0.05. The results showed that the extract, the ethylacetate fraction and the aqueous fraction (VUA) significantly increased the frequency of entry and the time spent on the open arm of the EPM at 50 and 100 mg/kg significantly, suggesting the anxiolytic-like activity. The open arm avoidance index further validated the anti-anxiety property of the extract and fractions. These effects were reversed by flumazenil, a GABAergic receptor antagonist (3 mg/kg), yohimbine (1 mg/kg), an antagonist of alpha₂-adrenergic receptor, and cyproheptadine (0.5 mg/kg), a serotonergic receptor antagonist. There was also an increase in the frequency of head dips at 50 (except VUA) and 100 mg/kg, suggesting an anti-anxiety-like effect of the extract and fractions in the hole-board model compared to the control. The study concluded that the extract, aqueous and ethylacetate fractions of V. unguiculata spp dekindtiana exhibited an anti-anxiety effect in mice which was probably mediated through GABAergic, α₂-adrenergic and serotonergic pathways.