【摘要】 本工作采用无血清培养的小鼠原代肝细胞制备了醋氨酚急性肝损伤模型，然后利用该模型观察了表皮生长因子（ＥＧＦ）对肝细胞的保护作用。结果如下：（１）小鼠原代肝细胞无血清培养液中加入终浓度为２０ｍｍｏｌ／Ｌ的醋氨酚培养１２－１４ｈ后，培养液中ＧＰＴ和ＧＰＴ的活性明显升高，可作为一种适当的肝细胞损伤模型。（２）提前１ｈ加入不同剂量（５０，１００，５００，１０００ｎｇ／ｍｌ）的ＥＧＦ可减轻醋氨酚引起的肝细胞损伤。（３）以３Ｈ－ＴｄＲ（３Ｈ－胸腺嘧啶核苷酸）参入为指标，可见醋氨酚使肝细胞ＤＮＡ合成速率明显降低，如预先加入ＥＧＦ，则可使之部分反转，但ＥＧＦ的保护作用与其刺激ＤＮＡ合成之间不存在正相关关系，因此ＤＮＡ合成的反转可能是ＥＧＦ对肝保护作用的结果而不是原因。（４）ＥＧＦ可增加正常肝细胞谷胱甘肽的含量，同时在一定程度上反转醋氨酚引起的ＧＳＨ含量的降低，由于ＧＳＨ在肝细胞实现解毒功能和增加其自身抗损伤能力方面具有重要作用，提示：ＥＧＦ的肝保护作用可能与其增强谷胱甘肽系统的功能有关。更多还原

【Abstract】 In the present work, the hepatoprotection of EGF was studied on an acetaminophen induced acute injury model of serum-free primary cultured mouse hepatocytes. The results were as follows: (1) When serum-free cultured mouse hepatocytes were exposed to acetaminophen (AAP 20 mmol/L) for 12-14 h, the activitiy of GPT and GOT were increased to a stable level, serving as a good hepetocyte injury model. (2) EGF of different doses (50, 100, 500, and 1000ng/ml) added to the medium prior to acetaminophen could reduce hepatocyte injury in a dose-dependent manner. (3) Taking 3H-TdR incorporation as an index, it was observed that acetuminophen could reduce the DNA synthesis of hepetocytes, and pretreatment with EGF could reverse this effect, but, stimulation of DNA synthesis by EGF was not correlated with its hepatoprotection. Thus the reversion of the reduced DNA synthesis in EGF-pretreated hepatocytes is interpreted as the result rather than the cause of cytoprotection of the factor. (4) The hepatoprotection might be produced through affecting on the glutathion metabolism of hepatocytes.更多还原