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表皮生长因子可抑制半胱胺诱导的大鼠十二指肠溃疡。

Epidermal growth factor inhibits cysteamine-induced duodenal ulcers in rats.

作者信息

Kunizaki C, Sugiyama M, Tsuchiya S

机构信息

Second Department of Surgery, Yokohama City University School of Medicine, Japan.

出版信息

Scand J Gastroenterol Suppl. 1989;162:218-21. doi: 10.3109/00365528909091165.

Abstract

We examined the pathogenesis of cysteamine-induced duodenal ulcers in rats, especially with reference to epidermal growth factor (EGF). Control, cysteamine (400 mg/kg, s.c.), cysteamine + EGF (20 micrograms/kg/day, i.p.) submandibular resection (SMR), SMR + cysteamine, and SMR + cysteamine + EGF groups were examined for duodenal ulceration. With submandibular resectioning, endogenous EGF decreased, and with the administration of EGF (i.p.), endogenous EGF increased. In the SMR + cysteamine group, serum gastrin increased and the intragastric pH decreased remarkably compared to in the normal control group. The administration of exogenous EGF suppressed this change. Mucosal blood flow, the potential difference and hexosamine, as defensive factors, decreased markedly in the SMR + cysteamine group, but the administration of exogenous EGF reversed these changes. These results suggested that a decrease in EGF is involved in the pathogenesis of cysteamine-induced duodenal ulcers in rats.

摘要

我们研究了半胱胺诱导的大鼠十二指肠溃疡的发病机制,尤其涉及表皮生长因子(EGF)。对对照组、半胱胺(400毫克/千克,皮下注射)组、半胱胺+EGF(20微克/千克/天,腹腔注射)组、下颌下腺切除(SMR)组、SMR+半胱胺组以及SMR+半胱胺+EGF组进行了十二指肠溃疡检查。随着下颌下腺切除,内源性EGF减少,而随着EGF(腹腔注射)的给药,内源性EGF增加。与正常对照组相比,SMR+半胱胺组血清胃泌素增加,胃内pH值显著降低。外源性EGF的给药抑制了这种变化。作为防御因子的黏膜血流量、电位差和氨基己糖在SMR+半胱胺组中显著降低,但外源性EGF的给药逆转了这些变化。这些结果表明,EGF的减少参与了半胱胺诱导的大鼠十二指肠溃疡的发病机制。

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