Key result
Artemisinin dose-dependently inhibits human platelet aggregation by downregulating PI3K/Akt and MAPK pathways.
Why the study?
Excessive platelet aggregation contributes to cardiovascular diseases, but the specific role and mechanisms of artemisinin on platelet activation and thrombus formation are not fully understood.
Does artemisinin inhibit U46619-induced platelet aggregation and granule secretion in human platelets?
Does artemisinin inhibit U46619-induced platelet aggregation and granule secretion in human platelets?
Effect estimate: IC50 326.31 μM
p-value: p=<0.05
Artemisinin demonstrates anti-platelet effects by inhibiting U46619-induced aggregation and granule secretion via downregulation of PI3K/Akt and MAPK pathways in human platelets.
Artemisinin shows potential antiplatelet activity in vitro; leaves open clinical translation and safety in humans.
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.
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Dong‐Ha Lee (2023) studied Platelet aggregation. Artemisinin vs. U46619-stimulated platelets was evaluated on U46619-induced platelet aggregation (IC50 326.31 μM, p=<0.05). Artemisinin dose-dependently inhibited U46619-induced human platelet aggregation with an IC50 of 326.31 μM by downregulating PI3K/Akt and MAPK pathways.
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