Related Experiment Video
Updated: Apr 25, 2026

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
Published on: April 6, 2017
A CAPE analogue as novel antiplatelet agent efficiently inhibits collagen-induced platelet aggregation
Objective:
Platelet activation plays a pivotal role in the pathogenesis of thrombosis, which can lead to fatal diseases such as myocardial or cerebral infarction, and atherosclerosis. The present study focused on investigating the effect of CAPE-NO2 against collagen-induced platelet aggregation.
Methods:
Caffeic acid phenethyl ester (CAPE) is an active component in propolis. CAPE-NO2 is a nitro derivative of CAPE. Its effects on rat platelet aggregation induced by collagen were tested in vitro and the potential mechanisms underlying the activities were investigated.
Results:
CAPE-NO2 significantly inhibited collagen-induced platelet aggregation in a concentration-dependent manner. It also reduced TXB2 formation and COX-1 activity in collagen-activated platelets. Moreover, CAPE-NO2 caused an increase in NO production and cGMP levels and attenuated 5-HT release in the collagen-activated platelets.
Conclusion:
These findings suggest that the inhibitory mechanism of CAPE-NO2 on collagen-induced platelet aggregation might be associated with the down-regulation of TXB2, COX-1 and 5-HT and the elevation of NO and cGMP production. These indicators are closely related to platelet function. So CAPE-NO2 may be a promising candidate for the extension of the current spectrum of antiplatelet drugs.
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...

