Nagakawa J, Hishinuma I, Hirota K, Miyamoto K, Yasuda M, Yamanaka T, Katayama K
Tsukuba Research Laboratories, Eisai Co., Ltd., Ibaraki, Japan.
Immunopharmacol Immunotoxicol. 1991;13(4):485-98. doi: 10.3109/08923979109019718.
The possible involvement of interleukin-1 alpha (IL-1 alpha) in the pathogenesis of murine hepatitis model induced with galactosamine and lipopolysaccharide (LPS) was investigated. The injection of 10 ng/mouse of LPS in combination with 10 mg/mouse of galactosamine into mice induced hepatic damage at 24 hours. Treatment with anti-mouse IL-1 alpha antiserum 30 min before galactosamine/LPS injection showed a tendency to reduce the liver injury, while pretreatment with anti-mouse tumor necrosis factor-alpha (TNF) antiserum significantly protected mice from liver injury. The use of recombinant murine TNF, instead of LPS, in combination with galactosamine could elicit hepatic damage, whereas recombinant murine IL-1 alpha could not substitute for LPS. However, recombinant murine IL-1 alpha enhanced the hepatotoxic effect of recombinant murine TNF in galactosamine-sensitized mice. These results suggest that TNF plays a major role in the pathogenesis of galactosamine/LPS hepatitis in mice and that IL-1 alpha acts synergistically with TNF in this hepatitis model.
研究了白细胞介素-1α（IL-1α）在半乳糖胺和脂多糖（LPS）诱导的小鼠肝炎模型发病机制中的可能作用。将10 ng/小鼠的LPS与10 mg/小鼠的半乳糖胺联合注射到小鼠体内，在24小时时诱导肝损伤。在注射半乳糖胺/LPS前30分钟用抗小鼠IL-1α抗血清治疗显示有减轻肝损伤的趋势，而用抗小鼠肿瘤坏死因子-α（TNF）抗血清预处理可显著保护小鼠免受肝损伤。用重组小鼠TNF代替LPS与半乳糖胺联合使用可引发肝损伤，而重组小鼠IL-1α不能替代LPS。然而，重组小鼠IL-1α增强了重组小鼠TNF对半乳糖胺致敏小鼠的肝毒性作用。这些结果表明，TNF在小鼠半乳糖胺/LPS肝炎的发病机制中起主要作用，并且IL-1α在该肝炎模型中与TNF协同发挥作用。
