Hirafuji M, Shinoda H
Department of Pharmacology, Tohoku University School of Dentistry, Sendai, Japan.
J Lipid Mediat. 1991 Nov;4(3):347-51.
N-formyl-methionyl-leucyl-phenylalanine (FMLP), but not leukotriene B4 (LTB4), induced a significant platelet adhesion to endothelial cell monolayer when polymorphonuclear leukocytes (PMNs) were present in vitro. Neither of FMLP and LTB4 had an effect on the platelet adhesion in the absence of PMNs. An antagonist of platelet-activating factor (PAF), WEB 2086 completely inhibited the platelet adhesion induced by FMLP, while indomethacin and AA-861 had no effect. These results suggest that PMN-dependent platelet adhesion to endothelial cells induced by FMLP is mediated by PAF, and that PAF plays an important role during cell-cell interactions among platelets, PMNs and endothelial cells.
在体外存在多形核白细胞（PMN）时，N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸（FMLP）可诱导血小板显著黏附于内皮细胞单层，而白三烯B4（LTB4）则无此作用。在不存在PMN的情况下，FMLP和LTB4对血小板黏附均无影响。血小板活化因子（PAF）拮抗剂WEB 2086可完全抑制FMLP诱导的血小板黏附，而吲哚美辛和AA-861则无作用。这些结果表明，FMLP诱导的PMN依赖性血小板与内皮细胞的黏附是由PAF介导的，且PAF在血小板、PMN和内皮细胞之间的细胞间相互作用中起重要作用。
