http://www.cnr.it/ontology/cnr/individuo/prodotto/ID313583
INHIBITION OF HUMAN PLATELET ACTIVATION AND AGGREGATION BY A NOVEL BIOISOSTER OF FLAVONOIDS (Abstract/Poster in atti di convegno)
- Type
- Label
- INHIBITION OF HUMAN PLATELET ACTIVATION AND AGGREGATION BY A NOVEL BIOISOSTER OF FLAVONOIDS (Abstract/Poster in atti di convegno) (literal)
- Anno
- 2013-01-01T00:00:00+01:00 (literal)
- Alternative label
Giulia Cigni1, S. Del Turco1, S. Sbrana1, D. Battaglia2, A. Papa2, C. La Motta3, S. Sartini3, G.
Basta1 (2013)
INHIBITION OF HUMAN PLATELET ACTIVATION AND AGGREGATION BY A NOVEL BIOISOSTER OF FLAVONOIDS
in 81st European Atherosclerosis Society Congress (EAS2013), Lyon, France, June 2-5, 2013
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Giulia Cigni1, S. Del Turco1, S. Sbrana1, D. Battaglia2, A. Papa2, C. La Motta3, S. Sartini3, G.
Basta1 (literal)
- Note
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- 1CNR Institute of Clinical Physiology, 2Fondazione Monasterio, CNR-Regione Toscana,
3Department of Pharmacy, University of Pisa, Pisa, Italy (literal)
- Titolo
- INHIBITION OF HUMAN PLATELET ACTIVATION AND AGGREGATION BY A NOVEL BIOISOSTER OF FLAVONOIDS (literal)
- Abstract
- Text: Aim. Platelets are the cause of formation of pathogenic thrombi in patients with atherothrombot
disease. This study was designed to investigate whether a novel bioisoster of flavonoid (named
DB103-F) prevents platelet activation and aggregation and thus, whether it may represent an
interesting agent to be used on drug eluting stents.
Methods. Human venous blood from healthy volunteers was collected in citrated tubes and
platelet activation was studied examining the P-selectin marker via flow cytometry. The platelet
aggregation was explored via a spectro-photometric assay. Platelet-rich plasma (300 x 109
platelets/L) incubated with increasing concentrations of DB103-F (12.5-25-50-100 ?mol/L) or
with DMSO alone were stimulated with the Thromboxane A2 (TXA2) mimetic U46619 (100-200
nmol/L for activation or 1-2 ?mol/L for aggregation), Collagen (10 ?g/mL), Thrombin (5 U/mL)
and ADP (10 ?mol/L).
Results. Platelet activation and aggregation induced by U46619 was significantly inhibited by
DB103-F in a concentration-dependent manner. The platelet inhibition of DB103-F correlated
with the ability of DB103-F to compete with the TXA2 receptor. Using U46619 at 200 nmol/L, the
IC50 of DB103-F was 30 ?mol/L. Further the ability of DB103-F to inhibit platelet activation and
aggregation induced by U46619 was independent by the time of pre-incubation with DB103-F
respect to the agonist.Further DB103-F was non-toxic on platelets until to 200 ?mol/L of
concentration and for long times of incubation, while quercetin or apigenin resulted already toxic
at 25 ?mol/L after one-half hour of incubation (toxicity evaluated with WST-1 assay). Using ADP
Collagen and Thrombin, the inhibition of platelet activation and aggregation by DB103-F was
unremarkable.
Conclusions. Clinically relevant concentrations of DB103-F affect platelet activation and
aggregation through a TXA2 receptor-dependent effect. Our findings support a role for DB103-F
as a novel drug to prevent the thrombotic complications of drug eluting stents.
Author Keywords: Platelet activation; drugs; atherothrombosis; flavonoids; thromboxane A2 . (literal)
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