DiJoseph J F, Wells C L
Division of Immunopharmacology, Wyeth-Ayerst Research, Princeton, NJ 08543-8000.
Agents Actions. 1989 Jun;27(3-4):294-6. doi: 10.1007/BF01972802.
Epidermal growth factor (EGF, 10 micrograms/kg po, ip, or sc, BID, and 20 micrograms/kg iv) had no protective activity in the indomethacin-induced intestinal lesion model (6 h model). In the ethanol-induced gastric lesion model, EGF (10 micrograms/kg sc) reduced lesions by 52% and reduced gastric acid secretion by 68% (5 micrograms/kg iv). In the 24 h indomethacin-induced intestinal lesion model, pretreatment with EGF (10 micrograms/kg sc, BID; 1 day before and during indomethacin treatment) had no beneficial effects. Therefore, EGF had no protective effects against non-steroidal antiinflammatory drug (NSAID)-induced intestinal lesions at doses that protect against the necrotizing action of ethanol and that inhibit gastric acid secretion in the rat.
表皮生长因子（EGF，经口、腹腔内或皮下注射，剂量为10微克/千克，每日两次，静脉注射剂量为20微克/千克）在吲哚美辛诱导的肠道损伤模型（6小时模型）中没有保护活性。在乙醇诱导的胃损伤模型中，EGF（皮下注射剂量为10微克/千克）使损伤减少了52%，胃酸分泌减少了68%（静脉注射剂量为5微克/千克）。在24小时吲哚美辛诱导的肠道损伤模型中，用EGF（皮下注射剂量为10微克/千克，每日两次；在吲哚美辛治疗前1天及治疗期间）进行预处理没有有益效果。因此，在能保护大鼠免受乙醇坏死作用并抑制胃酸分泌的剂量下，EGF对非甾体抗炎药（NSAID）诱导的肠道损伤没有保护作用。
