The role of leucocytes in the acetyl salicylic acid (aspirin) induced nitric oxide synthesis in the production of interferon-α, a potent inhibitor of platelet aggregation and a thrombolytic agent

• Published in: Journal of thrombosis and thrombolysis 2009-08, Vol.28 (2), p.173-184
• Main Authors: Bhattacharyya, Mau, Karmohapatra, Soumendra K., Bhattacharya, Gorachand, Bhattacharya, Rabindra, Sinha, A. Kumar
• Format: Article
• Language: English
• Subjects: Adenosine Diphosphate; Adult; Animals; Aspirin - pharmacology; Blood Platelets - metabolism; Cardiology; Cyclic AMP - metabolism; Cyclic GMP - metabolism; Female; Fibrin - metabolism; Fibrinolysis; Hematology; Humans; Interferon-alpha - biosynthesis; Leukocytes - metabolism; Male; Medicine; Medicine & Public Health; Mice; Middle Aged; Nitric Oxide - biosynthesis; Platelet Aggregation; Platelet Aggregation Inhibitors; Platelet-Rich Plasma - metabolism; Thrombosis - chemically induced; Thrombosis - metabolism
• ISSN: 0929-5305; 1573-742X
• DOI: 10.1007/s11239-008-0283-1

The role of aspirin-induced NO synthesis in the production of interferon-α (IFN-α) in leucocytes and the effect of IFN-α on platelet aggregation was studied. Treatment of Platelet Rich Plasma (PRP) with the dialyzed supernatant from the leucocyte suspension incubated with 80 μM aspirin resulted in parallel syntheses of NO and IFN-α as determined by methemoglobin assay and enzyme linked immunosorbent assay respectively. Incubation of PRP with 10 nM purified IFN-α for 40 min resulted in the maximal inhibition of platelet aggregation through the synthesis of NO due to the activation of nitric oxide synthase in platelets by IFN-α. The treatment of clotted PRP with IFN-α resulted in the lysis of the clot due to the fibrinolysis. Injection of IFN-α was found to protect mice from death due to the lysis of ADP-induced coronary thrombus. Interferon-α was found to be a potent inhibitor of platelet aggregation and a thromboprotective agent.