Thromb Haemost 2001; 86(05): 1284-1291
DOI: 10.1055/s-0037-1616063
Review Article
Schattauer GmbH

Thiosulfinates Inhibit Platelet Aggregation and Microparticle Shedding at a Calpain-dependent Step

Francine Rendu
1   U 428 INSERM, Faculté de Pharmacie, Université René Descartes Paris V, Paris
,
Brigitte Brohard-Bohn
1   U 428 INSERM, Faculté de Pharmacie, Université René Descartes Paris V, Paris
,
Sabine Pain
1   U 428 INSERM, Faculté de Pharmacie, Université René Descartes Paris V, Paris
,
Christilla Bachelot-Loza
1   U 428 INSERM, Faculté de Pharmacie, Université René Descartes Paris V, Paris
,
Jacques Auger
2   IRBI, Université François Rabelais, Tours, France
› Author Affiliations
We are grateful to Dr. P. Marche for his critical reading of the manuscript. S.P. was a recipient of Ministère de l'Education Nationale et de la Recherche. The work was supported by a grant from ARC (FR: 9545).
Further Information

Publication History

Received 25 November 2000

Accepted after resubmission 31 July 2001

Publication Date:
13 December 2017 (online)

Summary

Thiosulfinates (TSs) are sulfur compounds generated through the processing of different Allium species with antiplatelet property. To further define this platelet inhibitory effect we studied diallyl-TS (Al2TS), dipropyl-TS (Pr2TS), and dimethyl-TS (Me2TS) on platelet responses. The three TSs inhibited dose-dependent platelet aggregation, with IC50 values of 15 ± 2, 19 ± 2, and 9 ± 1 μM for Al2TS, Pr2TS and Me2TS, respectively. TSs had no effect on the expression of a platelet procoagulant surface, measured by flow cytometry as the binding of annexin V-FITC. They inhibited the microparticle shedding and clot retraction. Since the microparticle shedding is a calpain-activation dependent step, we assessed calpain activation by analysis of autoproteolysis in shorter active forms and by talin proteolysis in the presence of TSs. Calpain activation was inhibited by TSs independently of fibrinogen binding. Thus, TSs represent a new category of platelet inhibitors, acting on cal-pain-induced events.

 
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