Antithrombotic Effect of Artemisinin through Phosphoprotein Regulation in U46619-induced Platelets
Dong‐Ha Lee
Abstract
Normal activation of platelets and their aggregation are crucial during hemostasis process.It appears excessive or abnormal aggregation of platelets may bring about cardiovascular diseases like stroke, atherosclerosis, and thrombosis.For this reason, finding a substance that can regulate platelet aggregation or suppress aggregation will aid in the prevention and treatment of cardiovascular diseases.Artemisinin, a compound derived from Artemisia or Scopolia plants, has shown potential in various areas such as anticancer and Alzheimer's disease research.However, the specific role and mechanisms by which artemisinin influences platelet activation and thrombus formation are not yet fully understood.This study investigated the effects of artemisinin on platelet activation and thrombus formation.This study examined the effect of artemisinin on regulation of U46619-induced platelet aggregation, granule secretion.In addition, the effects of artemisinin on phosphorylation of PI3K/Akt and MAPK pathway involved in platelet aggregation was studied.As a result, artemisinin significantly downregulated of PI3K/Akt and MAPK pathway.In addition, artemisinin significantly reduced granule secretion, and platelet aggregation was inhibited by artemisinin.Therefore, we suggest that artemisinin is an anti-platelet substance that regulates PI3K/Akt and MAPK pathway and is valuable as a therapeutic and preventive agent for plateletderived cardiovascular disease.