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给予大鼠ｉｇ３－氧－乙酰－１１－脱氧甘草次酸铝（ＡＤＡ），５０，１００ｍｇ·ｋｇ－１，与阴性对照组相比，可显著降低对阿司匹林及应激性胃溃疡的溃疡面积，显著减少胃液量，降低胃液总酸度和胃蛋白酶活性；并且在相同剂量下，ＡＤＡ对阿司匹林和醋酸诱发胃溃疡的抑制作用显著比甘珀酸组强，同样ＡＤＡ还能显著增加胃内粘液量及胃壁内前列腺素Ｅ２（ＰＧＥ２）量．在醋酸型慢性胃溃疡模型中，ＡＤＡ１２５，２５０ｍｇ·ｋｇ－１（６２．５，１２５ｍｇ·ｋｇ－１，早晚各一次），连续１４ｄ，显著提高溃疡处胃粘膜血流量（ＧＭＢＦ）和溃疡治愈率，对血清钠，钾浓度无影响，相反甘珀酸可显著降低血清钾浓度．结果表明，ＡＤＡ可抑制溃疡形成及促进溃疡愈合，长期大剂量应用无甘珀酸引起的低血钾副作用，其抗溃疡机理可能与降低胃液总酸度，胃蛋白酶活性和促进胃粘液分泌，胃壁内ＰＧＥ２量及ＧＭＢＦ增加有关
Administration of ig3-oxo-acetyl-11-deoxyglycyrrhizate (ADA) at doses of 50 and 100 mg · kg-1 in rats significantly reduced the ulcer area of aspirin and stress ulcer compared with the negative control group, Significantly reduce the amount of gastric juice, reduce the total acidity of gastric juice and pepsin activity; and ADA on aspirin and acetic acid-induced gastric ulcer inhibition was significantly stronger than the group of the same, but also ADA significantly increased gastric mucus and Prostaglandin E2 (PGE2) levels in the stomach wall. ADA125, 250mg · kg-1 (62.5,125mg · kg-1, once a day, morning and evening) for 14 consecutive days significantly increased the gastric mucosal blood flow (GMBF) and ulcer cure rate in ulcer-induced chronic gastric ulcer model , Serum sodium and potassium concentration had no effect, on the contrary, carbenic acid can significantly reduce the serum potassium concentration. The results showed that ADA can inhibit ulcer formation and promote ulcer healing, long-term high-dose application of carbonic acid-induced hypokalemia side effects, the anti-ulcer mechanism may be associated with reducing gastric acidity, pepsin activity and promote gastric mucus secretion, stomach PGE2 volume and increased GMBF