Funaki N, Arii S, Adachi Y, Higashituji H, Fujita S, Furutani M, Mise M, Ishiguro S, Kitao T, Tanaka J
First Department of Surgery, Faculty of Medicine, Kyoto University, Japan.
Life Sci. 1992;51(17):1339-46. doi: 10.1016/0024-3205(92)90633-z.
In order to learn more about how human hepatic macrophages function, we analyzed the effect of exogenous PGE2 on the amounts of interleukin-1 (IL-1) and superoxide (O2-) released from primary-cultured human hepatic macrophages (HHM phi). When endogenous PGE2 production was blocked by indomethacin, exogenous PGE2 reduced IL-1 release from HHM phi in a dose-dependent manner, whereas it tended to increase O2- release from HHM phi. These results may suggest the probable contribution of PGE2 in regulating HHM phi mediator release in vivo.
为了更多地了解人类肝巨噬细胞的功能，我们分析了外源性前列腺素E2（PGE2）对原代培养的人类肝巨噬细胞（HHM phi）释放白细胞介素-1（IL-1）和超氧化物（O2-）量的影响。当内源性PGE2的产生被吲哚美辛阻断时，外源性PGE2以剂量依赖的方式减少HHM phi释放IL-1，而它倾向于增加HHM phi释放O2-。这些结果可能提示PGE2在体内调节HHM phi介质释放中可能发挥的作用。
