PI3K/Akt 및 MAPK 기전 조절을 통한 Artesunate의 콜라겐 유도의 사람 혈소판 응집 억제효과 = Artesunate inhibits collagen-induced human platelets aggregation through regulation of PI3K/Akt and MAPK pathway

다국어 초록 (Multilingual Abstract)

Excessive activation and aggregation of platelets is a major cause of cardiovascular disease. Therefore, inhibition of platelet activation and aggregation is considered an attractive therapeutic target in preventing and treating cardiovascular diseases. In particular, strong platelet activation and aggregation by collagen secreted from the vascular endothelium are characteristic of vascular diseases. Artesunate is a compound extracted from the plant roots of Artemisia or Scopolia species, and has been reported to be effective in anticancer and Alzheimer’s disease fields. However, the effect and mechanism of artesunate on collagen-induced platelet activation and aggregation have not been elucidated. In this study, the effect of artesunate on collageninduced human platelet aggregation was confirmed and the mechanism of action of artesunate was clarified. Artesunate inhibited the phosphorylation of PI3K/Akt and Mitogen-activated protein kinases, which are phosphoproteins that are known to act in the signal transduction process when platelets are activated. In addition, artesunate decreased TXA2 production and decreased granule secretion in platelets such as ATP and serotonin release.
As a result, artesunate strongly inhibited platelet aggregation induced by collagen, a strong aggregation inducer secreted from vascular endothelial cells, with an IC50 of 106.41 μM. These results suggest that artesunate has value as an effective antithrombotic agent for inhibiting the activation and aggregation of human platelets through vascular injury