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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.
Salix caprea
A European willow with salicin-rich bark used for pain, fever, and inflammatory conditions.
Salix caprea (goat willow) is a European willow species whose bark is rich in salicin and related salicylates, traditionally used for pain, fever, and inflammation. Modern evidence supports its analgesic and anti-inflammatory effects, though clinical data are limited (Evidence Level C). The primary active compounds include salicin, salicortin, catechins, and tannins.
Salicin is metabolized to salicylic acid, which inhibits cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis and thereby alleviating pain and inflammation. Additionally, flavonoids and catechins may provide antioxidant and anti-inflammatory effects through modulation of NF-κB and other inflammatory pathways. The antipyretic action is mediated via hypothalamic prostaglandin inhibition.
A European willow with salicin-rich bark used for pain, fever, and inflammatory conditions.
Salix caprea (goat willow) is a European willow species whose bark is rich in salicin and related salicylates, traditionally used for pain, fever, and inflammation. Modern evidence supports its analgesic and anti-inflammatory effects, though clinical data are limited (Evidence Level C). The primary active compounds include salicin, salicortin, catechins, and tannins.
Salicin is metabolized to salicylic acid, which inhibits cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis and thereby alleviating pain and inflammation. Additionally, flavonoids and catechins may provide antioxidant and anti-inflammatory effects through modulation of NF-κB and other inflammatory pathways. The antipyretic action is mediated via hypothalamic prostaglandin inhibition.