目的:探讨洛赛克抗胃溃疡的分子机理。方法:复制和幽门结扎胃溃疡大鼠模型,2mg/kg洛赛克连续给药5天,分别测溃疡指数、胃黏膜活性和胃液胃酸、CGRP含量、EGF分布和EGFR表达。结果:洛赛克可显著减小盐酸-乙醇胃溃疡模型大鼠胃黏膜溃疡指数(P<0.01),而对胃黏膜GSH含量和GSH-PX活性无显著影响(P>0.05);洛赛克可显著减小幽门结扎胃溃疡大鼠溃疡指数(P<0.01),抑制胃液量、游离酸、总酸度和总酸排出量的异常增加(P<0.01),增加胃黏膜CGRP含量和EGF分布(P<0.010),而对EGFR表达无显著影响(P>0.05)。结论:洛赛克抗盐酸-乙醇胃溃疡机制可能与GSH和GSH-PX介导的自基清除无关;抗幽门结扎胃溃疡机制可能与其强大的抑制胃酸胃液分泌、增加胃黏膜CGRP含量和EGF分布有关,而可能与胃黏膜EGFR表达无关。 Objective: To explore the molecular mechanism of Losec’s anti-gastric ulcer. Methods: The models of gastric ulcer were established by ligation and pylorus ligation. Losec at 2 mg / kg was given for 5 consecutive days. The ulcer index, gastric mucosal activity, gastric acid and CGRP content, EGF distribution and EGFR expression were measured. Results: Losec significantly reduced gastric mucosal ulcer index (P <0.01), but had no effect on GSH content and GSH-PX activity in gastric mucosa (P> 0.05). Losec (P <0.01), inhibit the abnormal increase of gastric juice, free acid, total acidity and total acid excretion (P <0.01), and increase the content of CGRP and EGF in gastric mucosa P <0.010), but had no significant effect on EGFR expression (P> 0.05). Conclusion: Losec’s anti-hydrochloric acid-ethanol gastric ulcer mechanism may be independent of GSH and GSH-PX mediated self-radical scavenging; anti-pyloric ligation gastric ulcer mechanism may be its strong inhibition of gastric acid and gastric secretion, increased gastric CGRP content and EGF distribution Which may not be related to gastric mucosal EGFR expression.