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近年证实胃泌素、表皮生长因子(EGF)和前列腺素(PG)可保护胃粘膜免遭包括应激在内的各种致溃疡刺激的损害,并增强粘膜细胞的增殖。由于应激可影响唾液腺生成EGP和胃粘膜生成PG,因此需要了解EGF和PG是否参与应激性溃疡的发生。作者以保留和切除唾液腺的大鼠为实验对象,研究了EGF在抵御浸水束缚应激试验(WRS)所致胃损伤中粘膜PG、巯基水平和细胞增殖的作用。材料与方法:雄性Wistar鼠5组,体重160～200g,禁食20小时。A组(80只)除对照亚组不作WRS试验即处死取材外,其余各亚组均于受试2、3、5、7、14小时后处死取材(胃粘膜、血)检测;B组分保留或切除唾液腺、试前用或未用EGF或PGE_2等亚组;C组接受WRS后形成溃疡,分试前用或未用消炎痛
In recent years, it has been confirmed that gastrin, epidermal growth factor (EGF) and prostaglandin (PG) can protect the gastric mucosa from damage caused by various ulceration stimuli including stress, and enhance the proliferation of mucosal cells. Since stress can affect the salivary glands to produce EGP and gastric mucosal PG production, it is necessary to understand whether EGF and PG are involved in the occurrence of stress ulcers. The authors studied rats with preserved and resected salivary glands, and studied the effects of EGF on mucosal PG, sulfhydryl levels, and cell proliferation in gastric mucosal lesions induced by WRS. Materials and Methods: Five male Wistar rats weighing 160-200 g were fasted for 20 hours. In group A (80 rats), except that the control group was sacrificed without WRS test, the other subgroups were killed at 2, 3, 5, 7, and 14 hours after the test (gastric mucosa and blood); Preservation or removal of salivary glands, pre-test or non-existence of EGF or PGE 2 subgroups; group C ulcers after WRS, with or without indomethacin prior to trial