洛赛克对胃溃疡大鼠胃黏膜保护作用与机理实验研究

Experimental Research of LOSEC on Gastric Mucosa Protection Function and Mechanism of Gastric Ulcer Big Rats

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：Explore the molecular mechanism of lose treatment on gastric ulcer.Methods：Copying and pyloric ligation induced gastric ulcer rat model,continuous medicine for five days.Respectively,measure the ulcer index,gastric mucosa activity and gastric acid,CGRP content,EGF distribution and EGFR expression.Results：Losec can significantly reduce gastric acid-ethanol rats of gastric mucosa ulcer index（P〈0.01）,yet gastric mucosal GSH content and GSH-PX activity had no significant influence（P〉0.05）.Losec can significantly reduce pyloric ligation induced gastric ulcer rat（P〈0.01）,restrain gastric acid,total amount,free acidity and total acids from abnormal increased（P〈0.01）,increase gastric mucosa CGRP content and distribution of EGF（P〈0.010）,but no significant effect of EGFR expression（P〉0.05）.Conclusion：The resistance mechanism on gastric acid-ethanol may have nothing to do with free radical scavenging of GSH and GSH-PX.The mechanism of antioxidant pyloric ligation may have relationship with its strong effect of inducing Gastric acid secretion,increasing gastric mucosa CGRP content and EGF distribution,but with no relevance to gastric mucosa EGFR expression.