entecavir and Thrombosis

Platelet activation is the primary cause of thrombosis. The P2X7 receptor (P2X7R) is a therapeutic target of thrombosis. However, it is still unknown whether P2X7R activation affects platelet thrombus. Our molecular docking results showed that entecavir as a P2X7R antagonist interacted perfectly with the human P2X7R (hP2X7R) in silico simulation studies. Furthermore, our experimental data revealed that entecavir could act as a P2X7R antagonist to exert cytoprotective effects against platelet activation via protecting mitochondrial function, improving lipid peroxidation and increasing antioxidant activity. Correlated with this, entecavir inhibited platelet aggregation, dense-granule secretion, P-selectin expression, integrin activation and Ca

Topics: Animals; Antioxidants; Bleeding Time; Blood Coagulation; Cytoprotection; Disease Models, Animal; Guanine; Humans; Lipid Peroxidation; Male; Mice, Inbred C57BL; Molecular Docking Simulation; Platelet Activation; Platelet Aggregation; Purinergic P2X Receptor Antagonists; Receptors, Purinergic P2X7; Thrombosis