Key result
Artocarpesin dose-dependently inhibited collagen-induced human platelet aggregation, reducing aggregation from 91.8% to 3.0% at 100 μM.
Why the study?
Platelets play a fundamental role in thrombosis and cardiovascular diseases, prompting the evaluation of natural substances such as artocarpesin isolated from Cudrania tricuspidata for antiplatelet effects.
Does artocarpesin inhibit platelet aggregation in human platelets in vitro?
Does artocarpesin inhibit platelet aggregation in human platelets in vitro?
Artocarpesin demonstrates in vitro antiplatelet and antithrombotic effects by modulating cyclic nucleotides and MAPKs, highlighting its potential as a therapeutic agent for cardiovascular diseases.
Answers are grounded in this paper and cite their sources.
Artocarpesin inhibits human platelet aggregation in vitro; this hypothesis-generating observation leaves open clinical antithrombotic potential.
The cardiovascular diseases (CVDs) are becoming a critical threat to our lives in these years. It is now widely accepted that platelets play an important role in cardiovascular disease as they have a fundamental role in thrombosis. Therefore, many drugs or natural substances have been developed to treat CVDs. Cudrania tricuspidata is a regional plant containing various constituents, such as xanthones, flavonoids, organic acids, and polysaccharides. It has been widely used in East Asia as an important ethnomedicine for the treatment of many diseases such as eczema, mumps, tuberculosis and acute arthritis. Therefore, we evaluated antiplatelet effects using artocarpesin isolated from C. tricuspidata. Confirmation of the antiplatelet function of artocarpesin was made according to the following analyzes. Artocarpesin inhibited collagen-induced human platelet aggregation, calcium mobilization, glycoprotein IIb/IIIa activation and thrombin-induced clot retraction through the regulation of associated signaling molecules. Artocarpesin increased the phosphorylation of vasodilator-stimulated phosphoprotein (VASP) and inositol 1, 4, 5-triphosphate receptor I (IP 3 RI). On the other hand, the phosphorylation of cytosolic phospholipase A 2 (cPLA 2 ), mitogen-activated protein kinases p38, JNK and phosphoinositide 3-kinase (PI3K)/Akt decreased. Thus, the study highlights that artocarpesin has an inhibitory effect on platelet activity and thrombus formation, showing its potential value in preventing platelet-induced cardiovascular disease.
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Kwon et al. (2022) studied Platelet aggregation. Artocarpesin vs. Collagen alone was evaluated on Collagen-induced human platelet aggregation (IC50 58.3 μM, p=<0.01). Artocarpesin dose-dependently inhibited collagen-induced human platelet aggregation, reducing aggregation from 91.8% to 3.0% at 100 μM.
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