Artemisinin inhibits collagen-induced human platelets aggregation through regulation of PI3K/Akt and MAPK pathway

The equilibrium of hemostasis is largely dependent on the controlled aggregation of platelets.However, the overaccumulation of platelets is a contributing factor to various cardiovascular complications, such as atherosclerosis, cerebral infarctions, and thrombotic conditions.Therefore, the search for agents that can regulate platelet clustering offers a viable strategy to either prevent or manage such health issues.Artemisinin, a compound sourced from plants such as Artemisia or Scoparia, has shown promise in various research domains, including the study of cancer and neurodegenerative diseases like Alzheimer's.Nevertheless, the exact processes through which it influences platelet clustering and the mechanism of action are not yet fully elucidated.Our study probed the effects of artemisinin on platelet activation, particularly its role in collagen-related platelet aggregation and the modulation of platelet granule release, focusing on its impact on the phosphorylation processes within the PI3K/Akt and MAPK pathways that are crucial to platelet aggregation.The results indicated a notable suppression of the PI3K/Akt and MAPK pathways activity following artemisinin treatment.Furthermore, artemisinin substantially decreased granule release and impeded platelet aggregation.These findings bolster the proposition that artemisinin can serve as an effective anti-platelet compound by modulating key signaling pathways, which may highlight its significant therapeutic and prophylactic potential against disorders related to platelet aggregation.