Studies on experimentally-induced acute hepatic failure

当将热灭活的痤疮丙酸杆菌（P. acnes）静脉注射到小鼠体内，7天后，还静脉注射少量的革兰氏阴性脂多糖（LPS）时，大多数小鼠死于大面积坏死。在该实验诱导的急性肝衰竭中，积聚到肝脏中的粘附细胞被痤疮丙酸杆菌引发并被LPS激活，产生细胞毒性因子。这种肝细胞毒性因子是一种蛋白质样物质，对热相对不稳定。此外，在本实验诱导的急性肝衰竭模型中，戈米辛A、AA 861、氮卓斯汀和前列腺素<E_1>均能显着提高小鼠的生存率，改善肝细胞的组织学变化和坏死。

When heat-killed Propionibacterium acnes (P. acnes) is intravenously injected into mice and seven days later, a small amount of gram-negative lipopolysaccharide (LPS) is also intravenously injected, most of the mice die of massive necrosis. In this experimentally-induced acute hepatic failure, the adherent cells accumulated into the liver are primed by P. acnes and activated by LPS, producing the cytotoxic factor. This hepatocytotoxic factor is a protein-like substance and is relatively unstable to heat. Furthermore, in this experimentally-induced acute hepatic failure model, gomisin A, AA861, azelastine and prostaglandin <E_1> remarkably increase the survival rate of mice and improve the histological changes and necrosis of the liver cells.