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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。
In this work, a model of acute hepatic injury induced by acetaminophen was prepared from mouse primary hepatocytes cultured in serum-free medium. Then the protective effect of epidermal growth factor (EGF) on hepatocytes was observed by this model. The results are as follows: (1) The activity of GPT and GPT in culture medium after incubation with acetaminophen at the final concentration of 20mmol / L for 12-14h in mouse primary hepatocyte serum-free medium can be used as a Appropriate models of hepatocellular injury. (2) Addition of EGF at different doses (50, 100, 500, 1000 ng / ml) 1 h earlier could reduce acetaminophen-induced hepatocellular injury. (3) The incorporation of 3H-TdR (3H-thymidine) into the index showed that acetaminophen significantly reduced the rate of DNA synthesis in hepatocytes. If EGF was added in advance, partial reversal could be made, but the protection of EGF There is no positive correlation between its role and its stimulation of DNA synthesis, so the reversal of DNA synthesis may be the result of EGF rather than liver protection rather than the reason. (4) EGF can increase the content of glutathione in normal liver cells, and at the same time, reverse the decrease of GSH content caused by acetaminophen to a certain extent. Since GSH has the ability of hepatocytes to detoxify and increase their own anti-injury ability Important role, Tip: EGF’s liver protective effect may be related to its enhanced glutathione system function.