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目的 探讨酸抑制剂对表皮生长因子（ＥＧＦ）活性的保护机理。方法用含有胃蛋白酶的盐酸培养重组人ＥＧＦ，用高压液相分析酸和胃蛋白酶中ＥＧＦ的稳定性，用３Ｈ－ＴｄＲ法测定酸降解的ＥＧＦ对胎肝细胞的体外生物活性的影响，用ＦＡＣＳ检测小鼠胎肝细胞经酸降解的ＥＧＦ诱导４８ｈ后ＥＧＦ的变化。结果所有含胃蛋白酶的标本中，当ｐＨ＜４．０时，ＥＧＦ被降解成为分子量较小的形式。经盐酸降解的该因子受体（ＥＧＦ）对小鼠胎肝细胞的增殖效应明显低于未用酸降解的ＥＧＦ处理组，未用酸降解的ＥＧＦ处理的小鼠胎肝细胞的ＥＧＦＲ表达也明显高于酸降解的ＥＧＦ处理组。结论 在ｐＨ＜４．０时，经酸处理的ＥＧＦ稳定性较差，能被迅速降解成分子量较小的形式，其活性也大大减弱，对小鼠胎肝细胞的促增殖作用明显低于未经酸降解的ＥＧＦ组。用抑酸药调节胃液中适当的ｐＨ值，对维持ＥＧＦ的稳定性，促进对胃粘膜的保护有一定作用。
Objective To investigate the protective mechanism of acid inhibitor on epidermal growth factor (EGF) activity. Methods Recombinant human EGF was cultured with pepsin-containing hydrochloric acid. The stability of EGF in acid and pepsin was analyzed by high pressure liquid chromatography. The effect of acid-degraded EGF on fetal liver cells in vitro was determined by 3H-TdR method. FACS The changes of EGF in 48 hours after acid-degraded EGF were detected in fetal rat hepatocytes. Results In all pepsin-containing samples, EGF was degraded to a lower molecular weight form at pH <4.0. The proliferation of mouse fetal hepatocytes induced by hydrochloric acid degradation of this factor receptor (EGF) was significantly lower than that of the untreated cells treated with acid, and the EGFR expression of mouse fetal hepatocytes without acid degradation was also significant Higher than acid-degraded EGF-treated group. Conclusion At pH <4.0, acid-treated EGF is poorly stable and can be quickly degraded into smaller molecular weight forms and its activity is greatly weakened. The effect of EGF on the proliferation of mouse fetal hepatocytes is significantly lower than that of untreated Acid-degraded EGF group. With acid-suppressing drugs to regulate the appropriate pH in gastric juice, to maintain the stability of EGF and promote gastric mucosal protection has a role.