Lapointe D S, Olson M S
Department of Biochemistry, University of Texas Health Science Center, San Antonio 78284-7760.
J Biol Chem. 1989 Jul 25;264(21):12130-3.
Platelet-activating factor (1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (AGEPC)) is a potent lipid mediator which stimulates hepatic glycogenolysis, causes hepatic vasoconstriction, and stimulates the production of cyclooxygenase-derived metabolites of arachidonic acid, primarily prostaglandin (PG) D2 in the perfused liver. Following infusion of platelet-activating factor (1 nM) in the perfused rat liver the production of PGD2, measured in the effluent perfusate, increased 4-fold after only 2 min. Infusion of the cyclooxygenase inhibitor, ibuprofen (50 microM), abolished the stimulated production of PGD2 and thromboxane B2 in response to AGEPC without significantly affecting the hepatic glycogenolytic or vasoconstrictive responses to AGEPC. Contrary to previous reports, these observations do not support the suggestion that cyclooxygenase-derived metabolites mediate directly either the glycogenolytic or the vasoactive effects of AGEPC in the perfused rat liver.
血小板活化因子（1-氧代十六烷基-2-乙酰基-sn-甘油-3-磷酸胆碱，即AGEPC）是一种强效脂质介质，可刺激肝糖原分解，引起肝血管收缩，并刺激花生四烯酸的环氧化酶衍生代谢产物的产生，在灌注肝脏中主要是前列腺素（PG）D2。在灌注的大鼠肝脏中注入血小板活化因子（1 nM）后，仅2分钟后，在流出的灌注液中测得的PGD2产量就增加了4倍。注入环氧化酶抑制剂布洛芬（50 microM）可消除AGEPC刺激的PGD2和血栓素B2的产生，而不会显著影响AGEPC对肝脏糖原分解或血管收缩的反应。与先前的报道相反，这些观察结果不支持环氧化酶衍生的代谢产物直接介导AGEPC在灌注大鼠肝脏中的糖原分解或血管活性作用的观点。
