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作者应用ABC免疫组织化学技术显示,奶油黄(DAB)、液氮致局部冻伤及CCl_4所致的3种肝损伤中也有细胞角蛋白(CK)异常表达肝细胞.①在肝局部冻伤及DAB性肝损伤模型中,表明不伴脂肪变性的肝细胞坏死不能直接引起肝细胞CK表达的改变;②在DAB性肝损伤中,肯定了卵园细胞对肝细胞CK表达改变的诱导作用,提出层粘连蛋白(LN)是卵园细胞产生的诱导物之一;③在CCl_4性肝炎及肝硬变中进行了CK和LN免疫细胞化学定位,表明肝细胞CK异常表达和LN异常沉积无论在位相上还是在时相上都密切相关,提出肝小叶结构破坏可能通过LN异常沉积而影响肝细胞的CK表达,LN等基底膜物质也是这一过程的诱导物;④在我们设计的一种局部肝冻伤模型上证实,肝细胞CK异常表达是肝小叶结构修复过程中肝细胞的适应性反应.
The authors used ABC immunohistochemical technique to show that cytokeratin (CK) abnormally expresses hepatocytes in three types of hepatic injury caused by cream yellow (DAB), liquid nitrogen, and CCl_4.1 Local frostbite and DAB in the liver In the hepatic injury model, hepatocyte necrosis without steatosis can not directly cause the alteration of CK expression in hepatocytes;2 In DAB hepatic injury, the induction of CK expression in hepatocytes by oocyte was confirmed, and layer adhesion was proposed. Protein (LN) is one of the inducers of ovary cell production; 3 immunocytochemical localization of CK and LN in CCl_4 hepatitis and cirrhosis, indicating abnormal expression of CK in liver cells and abnormal deposition of LN regardless of phase It is closely related to the time phase, suggesting that the destruction of the lobular structure may affect the expression of CK in hepatocytes through the abnormal deposition of LN, and basement membrane substances such as LN are also the inducers of this process;4 A local liver frostbite model we designed It was confirmed that the abnormal expression of CK in hepatocytes is an adaptive response of hepatocytes during hepatic lobular structure repair.