Key result
Pterostilbene cuts acute pulmonary thromboembolism mortality ~63% in mice without increasing bleeding time.
Why the study?
Development of therapeutic targets that prevent platelet activation is important to reduce cardiovascular disorders, and the inhibitory mechanisms of pterostilbene on platelets were not fully understood.
Does pterostilbene inhibit platelet activation in human platelets and reduce vascular thrombosis in mice?
Does pterostilbene inhibit platelet activation in human platelets and reduce vascular thrombosis in mice?
Absolute Event Rate: 37.5% vs 100%
Pterostilbene demonstrates potent antiplatelet activity in vitro and reduces thrombosis-related mortality in a mouse model without increasing bleeding risk.
PTE may inhibit thrombosis preclinically; leaves open any clinical antiplatelet role pending human trials.
Platelets play a crucial role in cardiovascular disorders (CVDs); thus, development of a therapeutic target that prevents platelet activation reduces CVDs. Pterostilbene (PTE) has several remarkable pharmacological activities, including anticancer and neuroprotection. Herein, we examined the inhibitory mechanisms of PTE in human platelets and its role in the prevention of vascular thrombosis in mice. At very low concentrations (1–5 μmol/L), PTE strongly inhibited collagen-induced platelet aggregation, but it did not have significant effects against thrombin and 9,11-dideoxy-11α,9α-epoxymethanoprostaglandin (U46619). PTE markedly reduced P-selectin expression on isolated α-granules by a novel microchip. Moreover, PTE inhibited adenosine triphosphate (ATP) release, intracellular ([Ca 2+ ]i) mobilization (resting, 216.6 ± 14.0 nmol/L; collagen-activated platelets, 396.5 ± 25.7 nmol/L; 2.5 μmol/L PTE, 259.4 ± 8.8 nmol/L; 5 μmol/L PTE, 231.8 ± 9.7 nmol/L), phospholipase C (PLC)γ2/protein kinase C (PKC), Akt, and mitogen-activated protein kinase (MAPK) phosphorylation. Neither 9-(tetrahydro-2-furanyl)-9 H -purin-6-amine (SQ22536) nor 1 H -[1,2,4]oxadiazolo[4,3- a ]quinoxalin-1-one (ODQ) reversed platelet aggregation inhibited by PTE. PTE did not affect vasodilator-stimulated phosphoprotein phosphorylation. In mice, PTE obviously reduced the mortality (from 100 to 37.5%) associated with acute pulmonary thromboembolism without increasing the bleeding time. Thus, PTE could be used to prevent CVDs.
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Huang et al. (2021) studied Cardiovascular disorders / vascular thrombosis. Pterostilbene was evaluated on Mortality associated with acute pulmonary thromboembolism. In mice, Pterostilbene reduced mortality associated with acute pulmonary thromboembolism from 100% to 37.5% without increasing bleeding time.
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