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Ce produit n'est pas destiné à diagnostiquer, traiter, guérir ou prévenir toute maladie. Ces déclarations n'ont pas été évaluées par la Food and Drug Administration.
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Ces informations sont fournies à titre éducatif uniquement et ne remplacent pas un avis médical professionnel, un diagnostic ou un traitement. Consultez toujours votre professionnel de santé avant d'utiliser des plantes, surtout si vous êtes enceinte, allaitez, prenez des médicaments ou avez une condition médicale.
Buthus martensii
TCM animal medicine from dried scorpion; used to extinguish wind and stop tremors; prescribed for epilepsy, stroke, facial paralysis, and rheumatic pain.
Quan Xie (Buthus martensii) is a traditional Chinese animal medicine derived from dried scorpion, used to extinguish wind and stop tremors. It is indicated for epilepsy, stroke, facial paralysis, and rheumatic pain. Key active compounds include buthotoxin, tityustoxin, and other neuroactive components that contribute to its antiepileptic, analgesic, and anti-inflammatory effects.
The primary mechanism involves modulation of voltage-gated sodium channels by neurotoxins such as buthotoxin and tityustoxin, leading to stabilization of neuronal membranes and anticonvulsant effects. Additionally, these compounds inhibit cyclooxygenase and lipoxygenase pathways, reducing prostaglandin and leukotriene synthesis, which contributes to analgesic and anti-inflammatory actions. The antispasmodic effects are mediated through interference with calcium ion channels and neurotransmitter release, particularly glutamate and GABA.
TCM animal medicine from dried scorpion; used to extinguish wind and stop tremors; prescribed for epilepsy, stroke, facial paralysis, and rheumatic pain.
Quan Xie (Buthus martensii) is a traditional Chinese animal medicine derived from dried scorpion, used to extinguish wind and stop tremors. It is indicated for epilepsy, stroke, facial paralysis, and rheumatic pain. Key active compounds include buthotoxin, tityustoxin, and other neuroactive components that contribute to its antiepileptic, analgesic, and anti-inflammatory effects.
The primary mechanism involves modulation of voltage-gated sodium channels by neurotoxins such as buthotoxin and tityustoxin, leading to stabilization of neuronal membranes and anticonvulsant effects. Additionally, these compounds inhibit cyclooxygenase and lipoxygenase pathways, reducing prostaglandin and leukotriene synthesis, which contributes to analgesic and anti-inflammatory actions. The antispasmodic effects are mediated through interference with calcium ion channels and neurotransmitter release, particularly glutamate and GABA.