Moodley I, Stuttle A
Prostaglandins. 1987 Feb;33(2):253-64. doi: 10.1016/0090-6980(87)90010-4.
The purpose of this study was to determine the role, if any, of Leukotriene B4 (LTB4) in Platelet Activating Factor (PAF)-induced aggregation of rat polymorphonuclear leucocytes (PMNs). Exposure of rat PMNs to 10(-7) M PAF resulted in the release of 4.5 +/- 0.7 ng/10(7) cells of LTB4 measured by radioimmunoassay. However, the maximum aggregation of PMNs achieved by exposure to LTB4 (10(-7)M) was only 50% of that produced by maximally aggregating concentrations of PAF (10(-7)M). 5-Lipoxygenase inhibitors, BW755c and Nafazatrom at concentrations that completely abolished LTB4 synthesis inhibited the aggregation induced by PAF only by 40% and 50% respectively. Furthermore, desensitisation experiments revealed that the aggregatory response of PMNs to PAF was only partially refractory to prior treatment with LTB4 whereas the aggregatory response to LTB4 was completely refractory to prior treatment with PAF. These results suggest that PAF-induced aggregation of rat PMNs is in part mediated by LTB4 and in part directly by an as yet unidentified mechanism.
本研究的目的是确定白三烯B4（LTB4）在血小板活化因子（PAF）诱导的大鼠多形核白细胞（PMN）聚集中是否发挥作用（若有作用）。通过放射免疫测定法检测，将大鼠PMN暴露于10⁻⁷M PAF会导致LTB4释放，释放量为4.5±0.7 ng/10⁷个细胞。然而，暴露于LTB4（10⁻⁷M）时PMN达到的最大聚集程度仅为最大聚集浓度的PAF（10⁻⁷M）所产生聚集程度的50%。5-脂氧合酶抑制剂BW755c和萘呋胺酯在完全消除LTB4合成的浓度下，分别仅抑制PAF诱导的聚集40%和50%。此外，脱敏实验表明，PMN对PAF的聚集反应仅部分抵抗LTB4的预处理，而对LTB4的聚集反应则完全抵抗PAF的预处理。这些结果表明，PAF诱导的大鼠PMN聚集部分由LTB4介导，部分由尚未明确的机制直接介导。
