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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.
Reseda luteola
European yellow dye plant used historically in folk medicine for skin conditions, anti-inflammatory, and fever.
Reseda luteola (weld) is a traditional dye plant historically used in European folk medicine for its anti-inflammatory, antipyretic, and skin-healing properties. Its primary active constituents include flavonoids such as luteolin, quercetin, and isorhamnetin, which contribute to its antioxidant and anti-inflammatory effects. Current evidence is limited (Level C), supporting its traditional uses but lacking robust clinical trials.
Luteolin and quercetin inhibit cyclooxygenase (COX) and lipoxygenase (LOX) pathways, reducing prostaglandin and leukotriene synthesis. They also suppress nuclear factor-kappa B (NF-κB) activation, decreasing pro-inflammatory cytokine production. The antipyretic effect may involve central prostaglandin inhibition, while antioxidant activity is mediated through free radical scavenging and upregulation of endogenous antioxidant enzymes.
European yellow dye plant used historically in folk medicine for skin conditions, anti-inflammatory, and fever.
Reseda luteola (weld) is a traditional dye plant historically used in European folk medicine for its anti-inflammatory, antipyretic, and skin-healing properties. Its primary active constituents include flavonoids such as luteolin, quercetin, and isorhamnetin, which contribute to its antioxidant and anti-inflammatory effects. Current evidence is limited (Level C), supporting its traditional uses but lacking robust clinical trials.
Luteolin and quercetin inhibit cyclooxygenase (COX) and lipoxygenase (LOX) pathways, reducing prostaglandin and leukotriene synthesis. They also suppress nuclear factor-kappa B (NF-κB) activation, decreasing pro-inflammatory cytokine production. The antipyretic effect may involve central prostaglandin inhibition, while antioxidant activity is mediated through free radical scavenging and upregulation of endogenous antioxidant enzymes.