Abstract
The mixture of water extracts from Tanacetum parthenium and Salix alba was studied in an ex vivo assessment of neurotoxicity constituted by isolated mouse cortex specimens challenged with K+ 60 mM Krebs–Ringer buffer (neurotoxicity stimulus). The effects of the mixture on lactate dehydrogenase (LDH), nitrite and serotonin levels were investigated. The phytochemical profile of the mixture was also evaluated. A docking approach was conducted to predict, albeit partially, the putative mechanism underlying the observed effects. The extracts displayed a good profile of polyphenolic compounds (22 chromatographic peaks detected), with caftaric acid and epicatechin being the prominent phenols. In isolated cortex, the association of T. parthenium and S. alba extracts was effective in reducing the K+ 60 mM-induced levels of LDH and nitrites, whereas the neurotoxicity stimulus-induced serotonin depletion was prevented by the treatment. Regarding the inhibition of serotonin catabolism, epicatechin (44.65 µg/mg) and caftaric acid (10.51 µg/mg) were putatively the main compounds involved in the inhibition of monoamineoxidase-A, which is known to play a master role in serotonin turnover. Collectively, the results of the present study point to the efficacy of the present extract mixture as an innovative pharmacological tool to prevent the onset of migraine.
Highlights
The results of the present study pointed to the efficacy of the mixture T. parthenium/S. alba, in an experimental model of migraine
The phytochemical profile is consistent with the inhibition of serotonin degradation, following cortex treatment, and the efficacy was demonstrated both in basal and neurotoxicity conditions, suggesting its use as both protection and prevention agent, in migraine
Based on the phytochemical composition, the inhibition of serotonin degradation could be related to the putative MAO-A inhibition by epicatechin and caftaric acid
Summary
Serotonin (5-HT) has long been involved in migraine etiopathogenesis, with clinical data pointing to tight relationships between neurotransmitter activity and migraine attacks [2]. 5-HT1B and 5-HT1D receptors could lead to the control of migraine attacks [3]; by contrast, the blockade of the 5-HT2A and 5-HT2C receptors was found effective in the prevention therapy [4]. Cortical spreading depression (CSD), a supraphysiological neurotoxicity stimulus, has been related to the migraine onset. CSD would represent a possible link between 5-HT depletion and trigeminal nociception [7]
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