Endo H, Akahoshi T, Kashiwazaki S
Department of Internal Medicine, Kitasato University School of Medicine, Kanagawa, Japan.
Biochem Biophys Res Commun. 1988 Oct 31;156(2):1007-14. doi: 10.1016/s0006-291x(88)80944-6.
The effect of interleukin 1 (IL-1) and tumor necrosis factor (TNF) on the induction of prostacyclin (PGI2) synthesis in human vascular endothelial cells (EC) was investigated. Both IL-1 and TNF increased PGI2 production by EC in both a time- and dose-dependent manner, and a combination of the two cytokines additively enhanced PGI2 production. Metabolic inhibitors including indomethacin and cycloheximide abolished cytokine induced PGI2 synthesis. Since, the effect of TNF was not inhibited by neutralization with antibody to IL-1 alpha and IL-1 beta, it seems that the mechanism is not mediated by endogenous IL-1 induced by TNF.
研究了白细胞介素1（IL-1）和肿瘤坏死因子（TNF）对人血管内皮细胞（EC）中前列环素（PGI2）合成诱导的影响。IL-1和TNF均以时间和剂量依赖性方式增加EC产生PGI2，并且两种细胞因子的组合可相加性增强PGI2的产生。包括吲哚美辛和环己酰亚胺在内的代谢抑制剂可消除细胞因子诱导的PGI2合成。由于TNF的作用不会被抗IL-1α和IL-1β抗体中和所抑制，因此其机制似乎不是由TNF诱导的内源性IL-1介导的。
