健脾益气中药对乙酸致胃溃疡大鼠氨基己糖及前列腺素E2的影响

目的：观察健脾益气中药对乙酸致胃溃疡大鼠胃组织中氨基己糖及前列腺素E2（PGE2）的影响，探讨健脾益气中药促进胃溃疡愈合的机制。方法：大鼠胃溃疡模型应用实验性乙酸法制备，随机分组，分别为空白对照组、模型组、健脾益气中药组和雷尼替丁组，连续给药治疗14天，采用酶联免疫法测定胃组织中PGE2的含量，用Morgan法原理测定胃组织氨基己糖。结果：与空白对照组大鼠比较，模型组大鼠胃组织PGE2含量明显降低（P〈0．01），雷尼替丁组大鼠PGE2没有明显变化（P〉0．05），健脾益气中药组大鼠PGE2明显升高（P〈0．05）；雷尼替丁组大鼠和健脾益气中药组大鼠比模型组大鼠均明显升高（P〈0．01）；健脾益气中药组大鼠胃组织PGE2明显高于雷尼替丁组大鼠（P〈0．05）。与空白对照组大鼠比较，模型组大鼠和雷尼替丁组大鼠氨基己糖含量明显降低（P〈0．01），健脾益气中药组大鼠没有明显变化（P〉0．05）；模型组大鼠与雷尼替丁组大鼠差异无显著性（P〉0．05），健脾益气中药组大鼠明显高于模型组大鼠（P〈0．05）；与雷尼替丁组大鼠相比健脾益气中药组大鼠明显升高（P〈0．05）。结论：健脾益气中药可以促进胃黏膜屏障的修复，使其防御功能接近正常水平，其机理可能是通过增加胃组织中氨基己糖、PGE2含量来完成的。

Effect of Chinese Drug of Jianpi Yiqi on Aminohexose and Prostaglandin E2 in Rats with Acetic Acid-induced Stomach Ulcer

Objective ： to observe the effect of Chinese drug of Jianpi Yiqi on aminohexose and Prostaglandin E2 in rats with acetic acid-induced stomach ulcer, and to explore the mechanism of the drug in improving the ulcer healing. Methods ： Prepare the model rats with stomach ulcer by experimental acetic acid method, dividing them into control group, model group, drug group and ranitidine group, with successive administration for 14 days. Euzymelinked immunosorbent assay was taken to determine the PGE2 content, and Morgan to determine the aminobexose in stomach tissues. Results ： Compared to control group, PGE2 was obviously decreased in model group （ P 〈0. 01） ; no obvious changes occurred in ranitidine group （ P 〉0. 05） ; PGE2 was obviously increased in drug group （ P 〈 0. 05 ） ; PGE2 in drug group was obviously higher than that in ranitidine group （ P 〈 0. 05 ） . Compared to control group, aminohexose in model group and ranitidine group significantly decreased （ P 〈 0. 01 ） ; no obvious changes occurred in drug group （ P 〉 0. 05 ） ; there was no significant difference between model group and ranitidine group （ P 〉 0.05 ） ; drug group was significantly higher model group （ P 〈 0. 05 ） ; aminohexose in drug group was significantly higher than that in model group （ P 〈 0. 05 ） . Conclusion ： Chinese drug of Jianpi Yiqi can promote the restoration of the stomach mucous membrane barrier and make its defense function approach to normal, leveL, whose mechanism may be accomplished by increasing the aminobexose and PGE2.