Murai A, Shimada H, Nakagawara G
First Department of Survery, Fukui Medical School.
Nihon Shokakibyo Gakkai Zasshi. 1996 Sep;93(9):620-7.
Focusing our attention on the TNF (tumor necrosis factor) produced by Kupffer cells (KCs). The role of KCs and polymorphonuclear neutrophils (PMNs) in endotoxin (LPS)-induced hepatocellular injury was investigated. This study used the culture fluid supernatant of KCs which had been stimulated with LPS as the "LPS stimulation supernatant", and evaluated hepatocellular injury as ornithine carbamyl transferase percent leakage. There was no difference between groups I (HCs: hepatocytes) and II (HCs + PMNs), but there were differences between groups I and III (HCs + LPS stimulation supernatant, groups II and IV (HCs + LPS stimulation supernatant + PMNs), and III and IV. There was no significant difference between III and V (III + anti-TNF antibody), but a difference was found between IV and VI (IV + anti-TNF antibody). These findings suggest that PMNs activated by KCs-generated TNF as well as KCs-derived humoral factors other than TNF play a role in the development of LPS-induced hepatocellular injury.
将我们的注意力集中在库普弗细胞（KCs）产生的肿瘤坏死因子（TNF）上。研究了库普弗细胞和多形核中性粒细胞（PMNs）在内毒素（LPS）诱导的肝细胞损伤中的作用。本研究使用经LPS刺激的库普弗细胞培养液上清液作为“LPS刺激上清液”，并将鸟氨酸氨甲酰基转移酶渗漏百分比作为肝细胞损伤的评估指标。第一组（HCs：肝细胞）和第二组（HCs + PMNs）之间无差异，但第一组和第三组（HCs + LPS刺激上清液）、第二组和第四组（HCs + LPS刺激上清液 + PMNs）以及第三组和第四组之间存在差异。第三组和第五组（第三组 + 抗TNF抗体）之间无显著差异，但第四组和第六组（第四组 + 抗TNF抗体）之间存在差异。这些发现表明，由库普弗细胞产生的TNF激活的多形核中性粒细胞以及除TNF之外的库普弗细胞衍生的体液因子在LPS诱导的肝细胞损伤发展中起作用。
