酒精性脂肪肝形成过程中肝细胞脂肪性病变的机制  

Mechanism of hepatic steatosis in alcoholic fatty liver disease formation

作　　者：王冬梅[1] 王兵 于聪[1] 吴琦[3] 李霞[1] 王向东[1] 

机构地区：[1]山东大学医学院细胞生物学研究所,济南250012 [2]潍坊高新区生物医药科技园,山东潍坊261000 [3]山东大学医学院人体解剖与组织胚胎学研究所,济南250012

出　　处：《山东大学学报（医学版）》2012年第7期19-25,共7页Journal of Shandong University:Health Sciences

摘　　要：目的研究乙醇引起肝细胞脂肪性病变的机制。方法以5 d龄KM乳小鼠肝细胞为实验材料,分为未分离纯化与分离纯化两大组原代培养,每大组均设正常对照组和乙醇实验组(50、100、200、300、400 mmol/L 5个乙醇浓度),采用形态学观察,油红O染色检测肝细胞脂肪变性的程度,RT-PCR检测PPARα与PPARγmRNA水平,以及TNF-α、IL-6mRNA水平的变化,综合评价乙醇引起细胞脂肪性病变的机制。结果未分离纯化的肝细胞发生了向脂肪细胞转变的现象;其PPARγ、TNF-α和IL-6的mRNA水平较其正常对照组有明显提高。结论纯化的肝细胞不易形成脂细胞;而乙醇处理肝脏细胞时,可能是肝细胞在非实质细胞及其产生的因子(包括免疫因子)的作用下发生了肝细胞脂肪变性即去分化或转分化的现象。Objective To study the mechanism of hepatic steatosis induced by ethanol. Methods Primarily cultured hepatocytes obtained from KM mouse at the 5th day were divided into two groups ： the primarily-cultured liver cells and the purified hepatocytes. Each group was divided into the control group and the experiment groups（50, 100, 200, 300 and 400 mmol/L of ethanol）. The hepatic steatosis degrees were evaluated by morphological changes and the oil red O staining. The changes of PPARα, PPARγ, TNF-α and IL-6 at mRNA level were tested with RT-PCR technique. Results The primarily-cultured liver cells underwent hepatic steatosis after the ethanol treatment, and the expressions of PPARγ, TNF-α and IL-6 at mRNA level improved obviously. Conclusion Purified hepatocytes lose the ability to trans-differentiate into fat cells. It is possible that the transdiferentiation of hepatocytes into fat cells is due to the ability of non-hepatocytes to provide some factors including immune factors upon ethanol stimulation：

关 键 词：脂肪肝 酒精性 肝细胞 脂肪变性 转分化 机制 

分 类 号：Q952.6[生物学—动物学]