Liu P, Wang Z Q, Zhang J
Department of Infectious Diseases, Second Hospital of China Medical University, Shenyang.
Zhonghua Nei Ke Za Zhi. 1994 Apr;33(4):241-3.
The protective effect of PGE1 in mice injected with propionibacterium acnes (P.acnes) and subsequently with a small dose of lipopoly-saccharide-endotoxin (LPS) 7 days later was studied. The results of this study were as follows: (1) When PGE1 was administered one hour before the injection of LPS, the survival rate of mice was significantly higher (90%), than that of a control group (17%). No necrosis was found in the liver. (2) PGE1 suppressed the release of tumor necrosis factor (TNF) and secreted-interleukin-1 (SIL-1) in culture supernatants of P.acnes-elicited kupffer cells and membrane IL-1 (mIL-1) in kupffer cells in a dose-dependent manner in vitro. These results strongly suggest that PGE1 can prevent liver cell necrosis in the animal model and the mechanism of curative effect of PGE1 in massive liver cell necrosis may result from inhibition of the activity of TNF, sIL-1 and mIL-1 in the kupffer cells.
研究了前列腺素E1（PGE1）对注射痤疮丙酸杆菌（P.acnes）并于7天后注射小剂量脂多糖内毒素（LPS）的小鼠的保护作用。本研究结果如下：（1）在注射LPS前1小时给予PGE1，小鼠存活率显著更高（90%），高于对照组（17%）。肝脏未发现坏死。（2）体外实验中，PGE1以剂量依赖方式抑制P.acnes诱导的库普弗细胞培养上清液中肿瘤坏死因子（TNF）和分泌型白细胞介素-1（SIL-1）的释放以及库普弗细胞中膜白细胞介素-1（mIL-1）的释放。这些结果有力地表明，PGE1可在动物模型中预防肝细胞坏死，PGE1对大规模肝细胞坏死的治疗作用机制可能源于其对库普弗细胞中TNF、sIL-1和mIL-1活性的抑制。
