Grundmann H J, Hähnle U, Hegenscheid B, Sahlmüller G, Bienzle U, Blitstein-Willinger E
Landesinstitut für Tropenmedizin, Humbolt University, Berlin, Germany.
J Infect Dis. 1992 Mar;165(3):501-5. doi: 10.1093/infdis/165.3.501.
Tumor necrosis factor (TNF), a protein produced in large quantities by endotoxin-activated macrophages, has been implicated as an important mediator of the lethal effect of endotoxin. A stable prostacyclin analogue (iloprost) was investigated for its ability to interfere with TNF secretion of lipopolysaccharide (LPS)-stimulated macrophages. It could be demonstrated by bioassays that LPS-induced TNF production was suppressed in a dose-dependent manner when macrophages were treated with iloprost at the time of LPS stimulation. Northern blot analysis revealed that iloprost inhibited TNF production at the transcription level. In vivo, endotoxin-induced mortality rates in galactosamine-sensitized mice could be significantly (P less than .05) reduced by iloprost administration. It is assumed that prostacyclin modulates endotoxin-induced and TNF-mediated inflammation in septic shock.
肿瘤坏死因子（TNF）是一种由内毒素激活的巨噬细胞大量产生的蛋白质，被认为是内毒素致死效应的重要介质。研究了一种稳定的前列环素类似物（依洛前列素）干扰脂多糖（LPS）刺激的巨噬细胞分泌TNF的能力。生物测定表明，在LPS刺激时用依洛前列素处理巨噬细胞，LPS诱导的TNF产生呈剂量依赖性抑制。Northern印迹分析显示依洛前列素在转录水平抑制TNF产生。在体内，给半乳糖胺致敏小鼠注射依洛前列素可显著（P<0.05）降低内毒素诱导的死亡率。推测前列环素可调节脓毒性休克中内毒素诱导的和TNF介导的炎症。
