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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.
Jacobaea vulgaris
European pasture weed highly toxic to livestock due to pyrrolizidine alkaloids; limited traditional human use.
Senecio jacobaea (Jacobaea vulgaris), commonly known as ragwort, is a toxic European pasture weed containing hepatotoxic pyrrolizidine alkaloids (PAs) such as jacobine and senecionine. Despite historical external use for wounds, its internal use is contraindicated due to severe hepatotoxicity and risk of veno-occlusive disease. Modern evidence is limited to toxicological studies, with no safe therapeutic application.
Pyrrolizidine alkaloids (PAs) are metabolically activated by hepatic cytochrome P450 enzymes (CYP3A4) to form reactive pyrrole metabolites that alkylate cellular macromolecules, leading to hepatocyte necrosis and sinusoidal endothelial cell damage. This results in veno-occlusive disease (VOD) characterized by occlusion of hepatic venules, fibrosis, and potentially fatal liver failure. PAs also inhibit DNA synthesis and induce apoptosis in hepatocytes.
European pasture weed highly toxic to livestock due to pyrrolizidine alkaloids; limited traditional human use.
Senecio jacobaea (Jacobaea vulgaris), commonly known as ragwort, is a toxic European pasture weed containing hepatotoxic pyrrolizidine alkaloids (PAs) such as jacobine and senecionine. Despite historical external use for wounds, its internal use is contraindicated due to severe hepatotoxicity and risk of veno-occlusive disease. Modern evidence is limited to toxicological studies, with no safe therapeutic application.
Pyrrolizidine alkaloids (PAs) are metabolically activated by hepatic cytochrome P450 enzymes (CYP3A4) to form reactive pyrrole metabolites that alkylate cellular macromolecules, leading to hepatocyte necrosis and sinusoidal endothelial cell damage. This results in veno-occlusive disease (VOD) characterized by occlusion of hepatic venules, fibrosis, and potentially fatal liver failure. PAs also inhibit DNA synthesis and induce apoptosis in hepatocytes.