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Lipoxin A augments release of thromboxane from human polymorphonuclear leukocyte suspensions
Author(s) -
Conti Pio,
Reale Marcella,
Cancelli Alessandro,
Angeletti Pietro U.
Publication year - 1987
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 - 10.1016/0014-5793(87)81139-0
Subject(s) - eicosanoid , chemistry , lipoxin , thromboxane , cyclooxygenase , thromboxane b2 , arachidonic acid , divalent , thromboxane a2 , lipoxygenase , ionophore , endogeny , biochemistry , pharmacology , platelet , enzyme , medicine , receptor , biology , membrane , organic chemistry
Lipoxin A (LXA) is a novel eicosanoid, generated by the interactions of lipoxygenases, which has a variety of biological actions. When added to human polymorphonuclear leukocytes, LXA stimulated thromboxane formation which was monitored as TxB2 by radioimmunoassay. The compound augmented the formation of TxA2 stimulated by the ionophore of divalent cations (A23187). Formation of thromboxane was inhibited by two non‐steroidal anti‐inflammatory drugs (i.e. indomethacin and proglumetacin). Results of the present study indicate that LXA can provoke the release and transformation of endogenous arachidonic acid to thromboxane. Moreover, they suggest a relationship between lipoxin A and the formation of cyclooxygenase pathway products.