Arii S, Monden K, 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). 1990;190(3):173-82. doi: 10.1007/pl00020020.
In the present study, the Kupffer cell function of rats with CCl4-induced liver cirrhosis was tested by analyzing the changes in the host defense system. In rats without liver cirrhosis injected with CCl4 for 3 weeks concomitant with the high opsonic activity the endocytic index was significantly increased. Rats treated for 9 and 13 weeks developed cirrhosis, and their endocytic indices were not increased despite the rise in their opsonic activity. Particularly, the endocytic index of 13-week-treated rats with advanced liver cirrhosis was significantly lower than that of the other groups. The organic distribution of 51Cr-endotoxin injected intravenously exhibited characteristic changes in 9-week- and 13-week-treated rats: decreased hepatic uptake and increased splenic uptake. In contrast, pulmonary uptake was increased in all CCl4-treated rats. The superoxide production by Kupffer cells from 13-week-treated rats was greatly reduced, accompanied by the decreased superoxide dismutase activity of liver homogenate. Thus, results of this study suggest that Kupffer cell dysfunction is one of the main factors affecting host defenses in liver cirrhosis.
在本研究中,通过分析宿主防御系统的变化来检测四氯化碳诱导的肝硬化大鼠的库普弗细胞功能。在未患肝硬化的大鼠中,注射四氯化碳3周并伴有高调理活性时,内吞指数显著增加。接受治疗9周和13周的大鼠出现了肝硬化,尽管其调理活性升高,但其内吞指数并未增加。特别是,接受治疗13周的晚期肝硬化大鼠的内吞指数明显低于其他组。静脉注射51Cr-内毒素后的器官分布在接受治疗9周和13周的大鼠中呈现出特征性变化:肝脏摄取减少,脾脏摄取增加。相比之下,所有接受四氯化碳治疗的大鼠肺部摄取均增加。接受治疗13周的大鼠库普弗细胞产生的超氧化物大大减少,同时肝脏匀浆中超氧化物歧化酶活性降低。因此,本研究结果表明,库普弗细胞功能障碍是影响肝硬化宿主防御的主要因素之一。