Monden K, Arii S, Itai S, Sasaoki T, Adachi Y, Funaki N, Higashitsuji H, Tobe T
First Department of Surgery, Kyoto University School of Medicine, Japan.
Res Exp Med (Berl). 1991;191(3):177-87. doi: 10.1007/BF02576673.
We investigated the production of chemical mediators by hepatic macrophages from rats with sepsis and the modulation of hepatocyte function by these hepatic macrophages. The chemical mediators we measured were superoxide (O2-), TNF, IL-1, and PGE2. Production of these mediators by hepatic macrophages from rats with sepsis was significantly increased. Furthermore, protein synthesis by cultured hepatocytes was inhibited in a co-culture system of hepatocytes and hepatic macrophages from rats with sepsis, and it was even inhibited by the supernatant of cultured hepatic macrophages from septic rats. These results demonstrate that hepatic macrophages are activated in sepsis and may play a role in inducing hepatic dysfunction in sepsis.
我们研究了脓毒症大鼠肝巨噬细胞产生化学介质的情况以及这些肝巨噬细胞对肝细胞功能的调节作用。我们检测的化学介质有超氧化物（O2-）、肿瘤坏死因子（TNF）、白细胞介素-1（IL-1）和前列腺素E2（PGE2）。脓毒症大鼠肝巨噬细胞产生这些介质的量显著增加。此外，在脓毒症大鼠肝细胞与肝巨噬细胞的共培养体系中，培养的肝细胞的蛋白质合成受到抑制，甚至脓毒症大鼠培养的肝巨噬细胞的上清液也能抑制其蛋白质合成。这些结果表明，肝巨噬细胞在脓毒症中被激活，可能在脓毒症诱导肝功能障碍中起作用。
