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Release of tumor necrosis factor-α and prostanoids in whole blood cultures after in vivo exposure to low-dose aspirin
Author(s) -
Ilse Beckmann,
Shlomo BenEfraim,
Monica Vervoort,
Henk C.S. Wallenburg
Publication year - 2001
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1080/09629350120054554
Subject(s) - prostanoid , aspirin , cyclooxygenase , thromboxane b2 , tumor necrosis factor alpha , cytokine , pharmacology , medicine , prostaglandin , thromboxane , in vivo , whole blood , endocrinology , chemistry , platelet , biology , biochemistry , enzyme , microbiology and biotechnology
The preventive effect of low-dose aspirin in cardiovascular disease is generally attributed to its antiplatelet action caused by differential inhibition of platelet cyclooxygenase-1. However, there is evidence that aspirin also affects release of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha). It is not known whether this is caused by direct action on the cytokine pathway or indirectly through cyclooxygenase inhibition and altered prostanoid synthesis, or both.

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