Xanthone impairs platelet activation and thrombus formation.

Area of Science:

• Biochemistry
• Pharmacology
• Hematology

Background:

• Xanthone, a Garcinia-derived compound, possesses diverse bioactivities.
• Its role in platelet function remains largely uncharacterized.

Purpose of the Study:

• To investigate the effects of xanthone on human platelet function.
• To evaluate xanthone's impact on hemostasis and thrombosis in vivo.

Main Methods:

• Human platelets were incubated with varying xanthone concentrations (0–20 μM).
• Platelet aggregation, granule release, activation, receptor expression, spreading, and clot retraction were analyzed.
• In vivo studies involved administering xanthone (10 mg/kg) to mice to assess hemostasis and thrombosis.

Main Results:

• Xanthone dose-dependently reduced platelet aggregation and granule release.
• It inhibited platelet spreading, clot retraction, and phosphorylation of key signaling molecules (c-Src, PLCγ2).
• In vivo, xanthone prolonged bleeding time and impaired arterial and venous thrombosis.

Conclusions:

• Xanthone impairs platelet activation and thrombus formation through multiple mechanisms.
• It inhibits signaling pathways including NF-κB, ERK1/2, p38, and calcium mobilization.
• Xanthone shows potential as a novel therapeutic agent for thrombotic and cardiovascular diseases.