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Prevention of αIIbβ3 activation by non‐steroidal antiinflammatory drugs
Author(s) -
Domı́nguez-Jiménez Carmen,
Dı́az-González Federico,
González-Álvaro Isidoro,
Cesar Jesús M.,
Sánchez-Madrid Francisco
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00236-7
Subject(s) - meloxicam , piroxicam , chemistry , aceclofenac , pharmacology , diclofenac , platelet activation , cyclooxygenase , aspirin , naproxen , platelet aggregation , platelet , mechanism of action , medicine , biochemistry , enzyme , in vitro , alternative medicine , chromatography , pathology
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.

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