Simmons P M, Salmon J A, Moncada S
Biochem Pharmacol. 1983 Apr 15;32(8):1353-9. doi: 10.1016/0006-2952(83)90446-x.
Leukotriene B4 (LTB4) has been detected by radioimmunoassay in inflammatory exudates obtained following the implantation of saline- or carrageenan-soaked polyester sponges in rats. The immunoreactive material was confirmed as LTB4 after extraction and purification by high pressure liquid chromatography. The peak concentration (6.9 +/- 0.5 ng/ml) was detected 6 hr after implantation of sponges soaked in 0.5% carrageenan; thereafter the level declined and was undetectable after 16-24 hr. The concentration of LTB4 during the early phase of the inflammatory response (4-8 hr) is sufficient to induce leukocyte aggregation, chemotaxis and degranulation of polymorphonuclear leukocytes (PMN) in vitro. Therefore, LTB4 may mediate, at least in part, the influx of PMN and contribute to other events which characterise the inflammatory response. The level of thromboxane B2 (TXB2) in the inflammatory exudate followed a similar time-course to that of LTB4 although the maximum concentration was higher (15-30 ng/ml). However, prostaglandin E2 (PGE2) exhibited a different time-course; the maximum level (20-30 ng/ml) was also reached 6-8 hr after implantation but remained elevated at 24 hr. The PMN count in the sponges and the concentrations of both LTB4 and TXB2, but not PGE2, were significantly reduced by prior treatment of the animals with colchicine. This suggests that PMN are the major source of LTB4 and TXB2 in the inflammatory exudate whereas PGE2 is produced in significant amounts by other tissues.
通过放射免疫分析法已在大鼠体内植入盐水或角叉菜胶浸泡过的聚酯海绵后获得的炎性渗出物中检测到白三烯B4(LTB4)。经高压液相色谱提取和纯化后,免疫反应性物质被确认为LTB4。在植入浸泡于0.5%角叉菜胶的海绵后6小时检测到峰值浓度(6.9±0.5纳克/毫升);此后水平下降,在16 - 24小时后无法检测到。炎症反应早期(4 - 8小时)LTB4的浓度足以在体外诱导白细胞聚集、趋化作用以及多形核白细胞(PMN)脱颗粒。因此,LTB4可能至少部分介导了PMN的流入,并促成了炎症反应的其他特征性事件。炎性渗出物中血栓素B2(TXB2)的水平与LTB4的时间进程相似,尽管最大浓度更高(15 - 30纳克/毫升)。然而,前列腺素E2(PGE2)呈现出不同的时间进程;最大水平(20 - 30纳克/毫升)也在植入后6 - 8小时达到,但在24小时时仍保持升高。用秋水仙碱预先处理动物后,海绵中的PMN计数以及LTB4和TXB2的浓度均显著降低,但PGE2未降低。这表明PMN是炎性渗出物中LTB4和TXB2的主要来源,而PGE2大量由其他组织产生。