3-氧-乙酰-11-脱氧甘草次酸铝抗大鼠实验性胃溃疡作用机制  

Antiulcer mechanism of aluminum 3-oxo-acetyl-11-deoxoglycyrrhetinate on experimental gastric ulcer in rats

作　　者：张玉林[1] 刘巨源[1] 杨锦南[1] 朱明[1] 刘春霞[1] 任京力[1] 

机构地区：[1]新乡医学院药理教研室,河南新乡453003

出　　处：《新乡医学院学报》2000年第1期5-6,9,共3页Journal of Xinxiang Medical University

基　　金：河南省教委资助项目

摘　　要：目的　探讨 3-氧 -乙酰 - 11-脱氧甘草次酸铝 (aluminum 3-oxo -acetyl- 11-deoxogly cyrrhetinate,ADA)对实验性大鼠胃溃疡的保护作用机制。 方法　采用Shay结扎法、醋酸法复制大鼠胃溃疡模型 ,分别测定给药后胃粘液PGE2 含量及胃粘膜血流量 (GMBF) ,并对结果进行统计分析。结果　ADA5 0mg·kg-1,10 0mg·kg-1与对照组相比 ,能显著增加胃内游离粘液和胃壁粘液量及胃壁内PGE2 含量(P <0 .0 1)。连续以ADA灌胃能显著增加胃粘膜血流量 (P <0 .0 1)。结论　ADA的抗溃疡作用与增加胃粘液量 ,促进PGE2Objective To research the protective effect and its mechanism of aluminum 3-oxo-acetyl-11-deoxoglycyrrhetinate (ADA) on experimental gastric ulcer in rats. Method Sparague-Dawley (SD) rats were replicated into gastric ulcer models by methods of pylous ligature and acetic acid. Gastric mucus content, gastric mucosal prostaglandin E 2 (PGE 2) and gastric mucosal blood flow (GMBF) were examined after drug respectively. The results were analyzed by statistic method. Results In compared with control group, ADA 50mg·kg -1 caused a significant increase in free and parietal mucus content (P<0.01) and markedly incresed the PGE 2 secretions of gastric mucosal (P<0.01). The consecutive administration of ADA (62.5mg·kg -1 , 125mg·kg -1 ) ig twice a day for 14d produced a significant increase in gastric mucosal blood flou (GMBF) (P<0.01).Conclusion The antiulcer action of ADA be related to increasing gastric mucus and PGE 2 secretion and GMBF.

关 键 词：脱氧甘草次酸铝 胃溃疡 粘液 前列腺素E2 

分 类 号：R975.6[医药卫生—药品]