Key result
Nifedipine markedly reduced fluorescein sodium-induced vessel thrombus formation in mice, an effect that was considerably inhibited by simultaneous administration of PPAR-β/-γ antagonists.
Why the study?
Does nifedipine reduce platelet aggregation and thrombus formation via PPAR-β/-γ-mediated signaling pathways in preclinical models?
Does nifedipine reduce platelet aggregation and thrombus formation via PPAR-β/-γ-mediated signaling pathways in preclinical models?
Nifedipine exhibits antiplatelet and antithrombotic activity through activation of PPAR-β/-γ-mediated signaling pathways, highlighting a novel mechanism for its cardiovascular benefits.
Supports antithrombotic effects of nifedipine via PPAR in mice; leaves open translation to human cardiovascular outcomes.
mobilization, PKCα activity, and surface glycoprotein IIb/IIIa expression caused by nifedipine. Thus, PPAR-β/-γ- dependent suppression of NF-κB activation also contributes to the antiplatelet activity of nifedipine. Consistently, administration of nifedipine markedly reduces fluorescein sodium-induced vessel thrombus formation in mice, which is considerably inhibited when the PPAR-β/-γ antagonists are administrated simultaneously. Collectively, these results provide important information regarding the mechanism by which nifedipine inhibits platelet aggregation and thrombus formation through activation of PPAR-β/-γ- mediated signaling pathways. These findings highlight that PPARs are novel therapeutic targets for preventing and treating platelet-hyperactivity-related vascular diseases.
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Tz‐Chong Chou (2014) studied Thrombus formation. Nifedipine vs. Nifedipine plus PPAR-β/-γ antagonists was evaluated on Vessel thrombus formation. Nifedipine markedly reduced fluorescein sodium-induced vessel thrombus formation in mice, an effect that was considerably inhibited by simultaneous administration of PPAR-β/-γ antagonists.
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