Ding Z, Li S, Wu Z
Department of Pathophysiology, Second Military Medical University, Shanghai, China.
Inflammation. 1992 Apr;16(2):179-86. doi: 10.1007/BF00918957.
Platelet-activating factor (PAF) stimulates leukocyte-endothelial cell (EC) adhesion through its effects either on leukocytes or on ECs. ECs may be injured, synthesize, or express new adhesive proteins to increase leukocyte adhesion. Intermediary mediators produced by activated ECs are also likely involved in promoting leukocyte adhesion. Our experiments demonstrated that PAF induced no obvious damage to bovine pulmonary artery ECs evaluated by lactic dehydrogenase release rate, angiotensin-converting enzyme activity, and cellular malondialdehyde content. Treatment of EC monolayers with 10(-9) M PAF increased polymorphonuclear leukocyte (PMN) adhesion. Increasing PAF concentration did not induce more PMN adherence. PAF elicited both a rapid and prolonged increment of PMN adherence to EC monolayers. The rapid adherence was greatly attenuated by pretreatment of ECs with PAF receptor antagonist SRI 63-441 but was not affected by pretreatment of PMNs with SRI 63-441, suggesting that PAF increases PMN adherence rapidly through its effects on specific receptors on ECs. Increased PMN adherence lasted if PAF treatment of ECs was sustained for 3 or 6 h. Pretreatment of ECs with actinomycin D, a protein synthesis inhibitor, significantly decreased PAF-induced sustained PMN adherence, but the inhibition is incomplete, suggesting that other mechanisms than protein synthesis also participated in the prolonged PMN adherence. We concluded from the results that PAF may induce both rapid and prolonged PMN adhesion to ECs. The effects are receptor mediated. The prolonged PMN adhesion is partly the result of protein synthesis.
血小板活化因子（PAF）通过其对白细胞或内皮细胞（EC）的作用刺激白细胞与内皮细胞的黏附。内皮细胞可能会受到损伤、合成或表达新的黏附蛋白以增加白细胞黏附。活化的内皮细胞产生的中间介质也可能参与促进白细胞黏附。我们的实验表明，通过乳酸脱氢酶释放率、血管紧张素转换酶活性和细胞丙二醛含量评估，PAF对牛肺动脉内皮细胞没有明显损伤。用10^(-9) M PAF处理内皮细胞单层可增加多形核白细胞（PMN）的黏附。增加PAF浓度并不会诱导更多的PMN黏附。PAF引起PMN对内皮细胞单层黏附的快速和持续增加。用PAF受体拮抗剂SRI 63 - 441预处理内皮细胞可大大减弱快速黏附，但用SRI 63 - 441预处理PMN则不影响快速黏附，这表明PAF通过其对内皮细胞上特定受体的作用快速增加PMN黏附。如果对内皮细胞持续进行3或6小时的PAF处理，PMN黏附增加会持续。用蛋白质合成抑制剂放线菌素D预处理内皮细胞可显著降低PAF诱导的PMN持续黏附，但抑制并不完全，这表明除了蛋白质合成外，其他机制也参与了PMN的持续黏附。我们从结果得出结论，PAF可能诱导PMN对内皮细胞的快速和持续黏附。这些作用是由受体介导的。PMN的持续黏附部分是蛋白质合成的结果。
