Breviario F, Proserpio P, Bertocchi F, Lampugnani M G, Mantovani A, Dejana E
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
Arteriosclerosis. 1990 Jan-Feb;10(1):129-34. doi: 10.1161/01.atv.10.1.129.
Interleukin-1 (IL-1) induced slow, lasting activation of human endothelial cells (EC) to release prostacyclin (PGI2). This was accompanied by endogenous 3H-arachidonic acid (3H-AA) release and by a time-dependent increase in the cells' ability to convert exogenous AA. The continuous presence of IL-1 was not required, but about a 1-hour stimulation with the cytokine was sufficient to trigger the cells to synthesize PGI2 for several hours. The spectrum of 3H-AA conversion shows that, in addition to 6-keto-prostaglandin F1 alpha, prostaglandin F2 alpha also was raised after IL-1. The recovery of PGI2 synthesis after aspirin was faster in IL-1-treated EC than in control cells. These data define some of the characteristics of IL-1 stimulation of PGI2 and suggest that this process is mediated both by endogenous AA mobilization and by an increase in cyclooxygenase activity.
白细胞介素-1（IL-1）可诱导人内皮细胞（EC）缓慢、持久地激活，从而释放前列环素（PGI2）。这伴随着内源性3H-花生四烯酸（3H-AA）的释放以及细胞转化外源性AA能力的时间依赖性增加。并不需要持续存在IL-1，但用该细胞因子刺激约1小时就足以触发细胞合成PGI2达数小时。3H-AA转化谱表明，除6-酮-前列腺素F1α外，IL-1作用后前列腺素F2α也升高。阿司匹林处理后，IL-1处理的EC中PGI2合成的恢复比对照细胞更快。这些数据确定了IL-1刺激PGI2的一些特征，并表明该过程是由内源性AA动员和环氧化酶活性增加介导的。
