Clopidogrel reduces platelet–leucocyte aggregation, monocyte activation and RANTES secretion in type 2 diabetes mellitus
Department of Cardiology, Wellington Hospital, Private Bag 7902, Wellington, New Zealand; scott.harding@ccdhb.org.nz
Department of Cardiology, Wellington Hospital, Private Bag 7902, Wellington, New Zealand; scott.harding@ccdhb.org.nz
Patients with diabetes mellitus have an increased risk of developing atherosclerosis and its sequelae. Atherosclerosis is an inflammatory disease involving multiple interactions between platelets, leucocytes and endothelial cells.1 Clopidogrel, a specific antagonist of the ADP P2Y12 receptor, inhibits both platelet activation and aggregation induced by ADP.2 Although clopidogrel has well‐documented antithrombotic actions, its potential anti‐inflammatory effects have been little investigated. We examined whether specific platelet inhibition with clopidogrel would reduce systemic inflammatory markers and specifically platelet, monocyte and endothelial activation in patients with type 2 diabetes mellitus.
Abbreviations
FITC - fluorescein isothiocyanate
PBS - phosphate‐buffered saline
PE - phycoerythrin
RANTES - regulated on activation normal T cell expressed presumed secreted
sCD40L - soluble CD40 ligand
Footnotes
Grant support: Drs Harding and Din were supported by grants from the British Heart Foundation (PG/2001/068; PG/03/009)
Competing interests: Professor Fox has received grant support for the Global Registry of Acute Coronary Events (GRACE) from Sanofi‐Aventis. All other authors have no conflict of interest to declare
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