Wang Y, Zhang X J
Department of Physiology, Beijing Medical University.
Sheng Li Xue Bao. 1994 Feb;46(1):8-16.
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 activity of GPT and GOT were increased to a stable level, serving as a good hepatocyte injury model. (2) EGF of different doses (50, 100, 500, and 1000 ng/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 acetaminophen could reduce the DNA synthesis of hepatocytes, 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 glutathione metabolism of hepatocytes.
在本研究中,在对乙酰氨基酚诱导的无血清原代培养小鼠肝细胞急性损伤模型上研究了表皮生长因子(EGF)的肝保护作用。结果如下:(1)当无血清培养的小鼠肝细胞暴露于对乙酰氨基酚(AAP 20 mmol/L)12 - 14小时时,谷丙转氨酶(GPT)和谷草转氨酶(GOT)活性升高至稳定水平,可作为良好的肝细胞损伤模型。(2)在加入对乙酰氨基酚之前向培养基中添加不同剂量(50、100、500和1000 ng/ml)的EGF可呈剂量依赖性地减轻肝细胞损伤。(3)以3H - 胸腺嘧啶核苷掺入为指标,观察到对乙酰氨基酚可降低肝细胞的DNA合成,而EGF预处理可逆转此效应,但EGF对DNA合成的刺激与其肝保护作用无关。因此,EGF预处理的肝细胞中DNA合成减少的逆转被解释为该因子细胞保护作用的结果而非原因。(4)肝保护作用可能是通过影响肝细胞的谷胱甘肽代谢产生的。