Garcia J G, Azghani A, Callahan K S, Johnson A R
Department of Biochemistry, University of Texas Health Center, Tyler.
Thromb Res. 1988 Jul 1;51(1):83-96. doi: 10.1016/0049-3848(88)90285-x.
The proinflammatory effects of platelet activating factor (PAF) that impact upon tissue inflammation were studied in vitro using the adherence of human neutrophils to endothelium and the increase in macromolecule permeability of endothelial monolayers. PAF produced both a time- and dose-dependent increase in neutrophil-endothelial cell adhesion. The adhesion promoting properties observed were primarily due to an effect of PAF on endothelium and not on neutrophils and was independent of endothelial cell cyclooxygenase products. The PAF receptor antagonist kadsurenone inhibited the adhesion response suggesting endothelial surface PAF receptors are involved in these responses. Whereas PAF alone did not alter endothelial cell barrier properties, leukocyte activation (neutrophil and platelets) with PAF produced significant increases in 125I-albumin clearance across endothelial monolayers. These studies suggest that PAF has potent proinflammatory effects and that it can play a significant role in the endothelial response to injury.
利用人中性粒细胞与内皮细胞的黏附以及内皮单层大分子通透性的增加，在体外研究了血小板活化因子（PAF）对组织炎症的促炎作用。PAF引起中性粒细胞与内皮细胞黏附呈时间和剂量依赖性增加。观察到的黏附促进特性主要是由于PAF对内皮细胞的作用，而非对中性粒细胞的作用，且与内皮细胞环氧化酶产物无关。PAF受体拮抗剂海风藤酮抑制了黏附反应，表明内皮表面的PAF受体参与了这些反应。虽然单独的PAF不会改变内皮细胞屏障特性，但PAF激活白细胞（中性粒细胞和血小板）会导致跨内皮单层的125I-白蛋白清除率显著增加。这些研究表明，PAF具有强大的促炎作用，并且在对损伤的内皮反应中发挥重要作用。
