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研究表皮生长因子（ＥＧＦ）对四氯化碳（ＣＣｌ４）所致大鼠原代培养肝细胞损伤的作用．方法：丙氨酸转氨酶（ＡｌａＡＴ）和天门冬氨酸转氨酶（ＡｓｐＡＴ）活力及Ｋ＋浓度用自动生化分析仪测定．丙二醛（ＭＤＡ）用苯巴比土酸比色法测定．放射活力用液体闪烁测量仪测定．细胞病理用光学显微镜和电子显微镜检查．结果：ＥＧＦ显著降低ＡｌａＡＴ，ＡｓｐＡＴ及ＭＤＡ水平，增加中毒肝细胞ＲＮＡ和ＤＮＡ的合成，且Ｋ＋漏出与ＤＮＡ的合成呈正相关．细胞病理显示ＥＧＦ减轻ＣＣｌ４对肝细胞的毒性作用．结论：ＥＧＦ对ＣＣｌ４所致原代培养肝细胞损伤有拮抗作用，肝细胞内Ｋ＋转运是ＤＮＡ合成起信息传递的启动因子．
To investigate the effect of epidermal growth factor (EGF) on primary cultured rat hepatocytes induced by carbon tetrachloride (CCl4). Methods: The activities of AlaAT and AspAT and K + concentration were measured by automatic biochemical analyzer. Malondialdehyde (MDA) was determined by phenobarbital acid colorimetry. Radioactivity was measured by a liquid scintillation meter. Cytopathology was examined by light microscopy and electron microscopy. Results: EGF significantly reduced the levels of AlaAT, AspAT and MDA, increased the synthesis of RNA and DNA in hepatocytes, and the leakage of K + was positively correlated with DNA synthesis. Cytopathology showed that EGF attenuated the toxic effects of CCl4 on hepatocytes. Conclusion: EGF can antagonize the injury of primary cultured hepatocytes induced by CCl4. K + transport in hepatocytes is the promoter of DNA synthesis.