McLeish K R, Wellhausen S R, Stelzer G T
Department of Medicine, University of Louisville School of Medicine, Kentucky.
Inflammation. 1987 Sep;11(3):279-88. doi: 10.1007/BF00915833.
In order to determine the mechanism of antiinflammatory activity, prostaglandin E2 (PGE2) or diluent was administered to rats 2 h prior to intradermal injections of various mediators of inflammatory vascular permeability changes. Vascular permeability was measured as the accumulation of [125I]rat serum albumin at the site of mediator injunction. PGE2 at 500 micrograms significantly inhibited protein leakage produced by histamine, platelet activating factor, zymosan, and zymosan-activated plasma. Pretreatment with PGE2 had no effect on protein leakage induced by injection of lysosomal enzymes, glucose oxidase, or xanthine oxidase. The accumulation of polymorphonuclear leukocytes (PMNs) at the site of injection of zymosan or zymosan-activated plasma was not altered by PGE2 administration. In separate experiments, the ability of PGE2 to alter phagocytosis and oxygen radical production by PMN was examined. PGE2 significantly inhibited phagocytosis at 2 h, but this returned to normal by 6 h. Production of hydrogen peroxide by PMN was not affected by PGE2. These results suggest that PGE2 prevents acute changes in vascular protein leakage by preventing endothelial cell contraction and by inhibiting specific PMN functions.
为了确定抗炎活性的机制，在皮内注射各种炎症性血管通透性变化介质前2小时，给大鼠注射前列腺素E2（PGE2）或稀释剂。血管通透性通过[125I]大鼠血清白蛋白在介质注射部位的蓄积来测定。500微克的PGE2显著抑制组胺、血小板活化因子、酵母聚糖和酵母聚糖激活血浆所产生的蛋白质渗漏。PGE2预处理对注射溶酶体酶、葡萄糖氧化酶或黄嘌呤氧化酶诱导的蛋白质渗漏没有影响。PGE2给药并未改变酵母聚糖或酵母聚糖激活血浆注射部位多形核白细胞（PMN）的蓄积。在单独的实验中，检测了PGE2改变PMN吞噬作用和氧自由基产生的能力。PGE2在2小时时显著抑制吞噬作用，但在6小时时恢复正常。PMN产生过氧化氢不受PGE2影响。这些结果表明，PGE2通过防止内皮细胞收缩和抑制特定的PMN功能来预防血管蛋白质渗漏的急性变化。
