Prevention of αIIbβ3 activation by non‐steroidal antiinflammatory drugs

FEBS Letters

Domı́nguez-Jiménez, Carmen³  González-Álvaro, Isidoro²  Cesar, Jesús M.¹  Sánchez-Madrid, Francisco³  Dı́az-González, Federico² 

[1] Servicio de Hematologı́a of Hospital Ramón y Cajal, ctra. de Colmenar Km 9,1, 28034 Madrid, Spain;Servicio de Reumatologı́a of Hospital de la Princesa, Universidad Autónoma de Madrid, Diego de León 62, 28006 Madrid, Spain;Servicio de Inmunologı́a of Hospital de la Princesa, Universidad Autónoma de Madrid, Diego de León 62, 28006 Madrid, Spain

关键词: Non-steroidal antiinflammatory drug;    αIIbβ3;    Platelet activation;    DMSO;    dimethyl sulfoxide;    mAb;    monoclonal antibody;    NSAIDs;    non-steroidal antiinflammatory drugs;    PGI2;    prostaglandin I2;    PRP;    platelet rich plasma;    TXB2;    thromboxane B2;   

DOI  :  10.1016/S0014-5793(99)00236-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

We have studied the effect of non-steroidal antiinflammatory drugs (NSAIDs) on αIIbβ3 integrin activation and platelet aggregation. NSAIDs such as meloxicam, piroxicam, indomethacin and aspirin, but not aceclofenac or diclofenac interfered with the activation state of αIIbβ3. NSAIDs that inhibited αIIbβ3 activation were also able both to partially inhibit platelet primary aggregation and to accelerate platelet deaggregation. These effects of NSAIDs were not dependent on cyclooxygenase inhibition. The results obtained indicate that some NSAIDs exert a specific action on αIIbβ3 activation, and provide an additional mechanism that accounts for their beneficial effects in diseases in which platelet activation is involved.

【 授权许可】

Unknown