十二指肠胃反流大鼠胃黏膜氨基己糖、磷脂、PGE_2的变化  

Changes of hexosamine,phospholipids,PGE2 in gastric mucosa of model rats with duodenogastric reflux

作　　者：杨华[1] 龚均[2] 

机构地区：[1]西安市第一医院干部病房消化科,西安710002 [2]西安交通大学医学院第二附属医院

出　　处：《陕西医学杂志》2012年第2期131-132,161,共3页Shaanxi Medical Journal

基　　金：卫生部临床学科重点项目(No:20012130)

摘　　要：目的:观察十二指肠胃反流大鼠胃黏液凝胶层、胃黏膜氨基己糖、磷脂、前列腺素E2(PGE2)含量的变化。方法:将SD大鼠分为对照组和造模组,造模组以手术建立大鼠十二指肠反流性胃炎(DGR)模型,每日给予生理盐水灌胃1次。8周后对大鼠胃标本进行病理学检查,观察胃黏膜损伤指数(UI)和胃凝胶黏液层厚度,测定胃黏膜氨基己糖、磷脂的含量,放射免疫法检测胃黏膜前列腺素E2(PGE2)水平。结果:对照组胃黏膜病理改变明显轻于DGR组,胃黏膜UI明显低于DGR组(P<0.01);DGR组胃黏液凝胶层厚度、胃黏膜氨基己糖、磷脂和前列腺素E2含量均显著低于对照组(P<0.01)。结论:胃黏液的合成减少,糖蛋白和脂质的破坏增加以及内源性PGs的生成减少是DGR时造成胃黏膜屏障损伤的原因之一。Objective：To investigate the changes of hexosamine,phospholipids,PGE2 in gastric mucosa in duodenogastric refluent rats.Methods：The SD rats were divided into normal control group and model group,and duodenogastric refluent rat models were established by operation.Model group were treated orally by 0.9% brine everyday.The gastric specimens in rats were examined by pathology after 8 weeks.The gastric mucosa of the gastric ulcer index（UI）,the thickness of gastric gelatinous mucus,the gastric hexosamine and phospholipids were detected.The level of gastric mucosal PGE2 was measured by radioimmunoassay.Results：The histological change and gastric UI in normal control group were apparently less than those in model group（P〈0.01）.In DGR group,the thickness of gastric gelatinous mucus,the content of gastric hexosamine and phospholipids,and level of gastric PGE2 were apparently less than those in normal control group（P〈0.01）.Conclusion：It is one of the reasons that synthesis of gastric mucus reduces,breakage of glycoprotein and lipide increases,and synthesis of endogenous prostaglandins reduces in the duodenogastric reflux model in rats.

关 键 词：十二指肠胃反流/病因学 胃黏膜/损伤 氨基糖类/代谢 磷脂类/代谢 16 16-二甲基前列腺素E2/代谢 

分 类 号：R574.4[医药卫生—消化系统]