Hotter G, Closa D, Prats N, Pi F, Gelpí E, Roselló-Catafau J
Department of Medical Bioanalysis, Institut d'Investigacions Biomèdiques de Barcelona, CSIC, Spain.
Free Radic Biol Med. 1997;22(6):947-54. doi: 10.1016/s0891-5849(96)00494-7.
In the present investigation we studied the concerted role of superoxide anion, platelet activating factor (PAF) and leukotriene B4 (LTB4) in the mechanism that results in polymorphonuclear leucocyte accumulation induced by oxygen free radicals in rat pancreas. This was done by comparing the effects of a PAF antagonist (BN-52021), a LTB4 inhibitor (MK-886) and superoxide dismutase (SOD) in a experimental rat model of inflammation elicited by the oxygen free radicals induced via infusion of xanthine/xanthine oxidase. Also, the effect of independent LTB4 infusion has been studied. The results show that increases in polymorphonuclear cell infiltration (evaluated by tissue histology), myeloperoxidase and LTB4 levels induced in pancreas by infusion of xanthine/xanthine oxidase were abolished by the administration of either the PAF antagonist, the LTB4 inhibitor, or SOD. The fact that BN-52021 could prevent neutrophil recruitment and LTB4 synthesis suggests that PAF is a necessary step for subsequent LTB4 synthesis and polymorphonuclear leucocyte accumulation.
在本研究中，我们研究了超氧阴离子、血小板活化因子（PAF）和白三烯B4（LTB4）在大鼠胰腺中由氧自由基诱导的多形核白细胞积聚机制中的协同作用。这是通过比较PAF拮抗剂（BN - 52021）、LTB4抑制剂（MK - 886）和超氧化物歧化酶（SOD）在由黄嘌呤/黄嘌呤氧化酶输注诱导的氧自由基引发的实验性大鼠炎症模型中的作用来完成的。此外，还研究了单独输注LTB4的效果。结果表明，通过给予PAF拮抗剂、LTB4抑制剂或SOD，可消除由黄嘌呤/黄嘌呤氧化酶输注诱导的胰腺中多形核细胞浸润（通过组织病理学评估）、髓过氧化物酶和LTB4水平的升高。BN - 52021能够阻止中性粒细胞募集和LTB4合成这一事实表明，PAF是随后LTB4合成和多形核白细胞积聚的必要步骤。
