<p>Thrombosis is a leading cause of cardiovascular diseases, driven by platelet aggregation, endothelial activation, and vascular occlusion. While <i>Allium cepa</i> L. (onion) is known for its health benefits, the antithrombotic potential of its peel remains underexplored. This study investigates the effects of <i>Allium cepa</i> L. peel extract (APE) in a rat model of collagen and epinephrine (CE)-induced thrombosis. High-performance liquid chromatography confirmed that APE contains high levels of quercetin, a flavonoid with known vascular protective properties. Animal experiments showed that APE significantly prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), indicating decreased hypercoagulability. Furthermore, APE suppressed genetic expression of key adhesion molecules (ICAM-1, VCAM-1, P-selectin, and E-selectin) in aortic tissue, suggesting reduced endothelial activation. Histological analysis also demonstrated a decrease in pulmonary vascular occlusion. These results suggest that APE may help prevent thrombosis by regulating coagulation and protecting endothelial function, supporting its potential as a natural antithrombotic agent.</p>

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Allium cepa L. (onion) peel alleviates collagen and epinephrine-induced thrombosis in rats

  • Hye In Nam,
  • Ardina Nur Fauziah,
  • Heeju Kim,
  • Geon Jeong,
  • Minha Oh,
  • Sung Keun Jung,
  • Ji Yeon Kim,
  • Young Jun Kim,
  • Hong Jin Lee,
  • Sanguine Byun

摘要

Thrombosis is a leading cause of cardiovascular diseases, driven by platelet aggregation, endothelial activation, and vascular occlusion. While Allium cepa L. (onion) is known for its health benefits, the antithrombotic potential of its peel remains underexplored. This study investigates the effects of Allium cepa L. peel extract (APE) in a rat model of collagen and epinephrine (CE)-induced thrombosis. High-performance liquid chromatography confirmed that APE contains high levels of quercetin, a flavonoid with known vascular protective properties. Animal experiments showed that APE significantly prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT), indicating decreased hypercoagulability. Furthermore, APE suppressed genetic expression of key adhesion molecules (ICAM-1, VCAM-1, P-selectin, and E-selectin) in aortic tissue, suggesting reduced endothelial activation. Histological analysis also demonstrated a decrease in pulmonary vascular occlusion. These results suggest that APE may help prevent thrombosis by regulating coagulation and protecting endothelial function, supporting its potential as a natural antithrombotic agent.