Neuroprotective properties of Valeriana officinalis extracts (original) (raw)

Valeriana officinalis have been used in traditional medicine for its sedative, hypnotic, and anticonvulsant effects. There are several eports in the literature supporting a GABAergic mechanism of action for valerian. The rationale of the present work is based on the concept that by decreasing neuronal network excitability valerian consumption may contribute to neuroprotection. The aim of our investigation was to evaluate the neuroprotective effects ofV. officinalis against the toxicity induced by amyloid beta peptide 25–35 [Aβ(25–35)]. Cultured rat hip-pocampal neurons were exposed to Aβ(25–35)(25 μM) for 24–48 h,after which morphological and biochemical properties were evaluated. The neuronal injury evoked by Aβ, which includes a decrease in cell educing capacity and associated neuronal degeneration, was prevented by valerian extract. Analysis of intracellular free calcium ([Ca2+]i)indicated that the neuroprotective mechanisms may involve the inhibition of excess influx of Ca2+ following neuronal injury. Moreover, membrane peroxidation in rat hippocampal synaptosomes was evaluated, and our data indicate that valerian extract partially inhibited ascorbate/iron-induced peroxidation. In conclusion we show evidence that the signalling pathways involving [Ca2+]i and the redox state of the cells may play a central ole in the neuroprotective properties ofV. officinalis extract against Aβ toxicity. The novelty of the findings of the present work, indicating neuroprotective properties of valerian against Aβ toxicity may, at the long-term, contribute to introduction of a new elevant use of valerian alcoholic extract to prevent neuronal degeneration in aging or neurodegenerative disorders.