摘要
【目的】探讨十二指肠胃反流 (DGR)引起大鼠胃黏膜损伤及癌变的发病机制。【方法】健康成年雄性SD大鼠 (75只 )随机分为两组。①DGR模型组 (5 5只 ) :根据手术造模方式及反流量大小分为全反流组与部分反流组 ;②假手术对照组 (2 0只 ) :采用 pH监测仪测定胃液 pH ,用酶法测定胃液胆汁酸 (TBA) ,确定DGR模型成功。进行为期 3个月和 9个月胃黏膜损伤的动态观察。S P分析不同病变胃黏膜组织CyclinD1、p16蛋白的表达。【结果】DGR模型大鼠胃液pH及TBA明显升高 (P <0 .0 1) ,证明DGR模型成功。模型大鼠病理改变出现浅表性胃炎→萎缩性胃炎→异型增生的动态演变过程。萎缩性胃炎组及异型增生时CyclinD1蛋白表达显著高于假手术对照组及浅表性胃炎组 (P <0 .0 5 ) ,癌基因CyclinD1为高表达。在萎缩性胃炎与异型增生之间CyclinD1表达差异无显著性 (P >0 .0 5 )。而 p16蛋白表达则相反 ,在假手术对照组最高 ,在异型增生最低 ,两组之间差异有显著性 (P <0 .0 1) ,p16在异型增生时为低表达。CyclinD1与 p16表达呈负相关。【结论】CyclinD1、p16蛋白表达异常是DGR胃黏膜损伤及癌变的分子机制之一。
Objectives]To explore the pathogenesis of cell injury and canceration in gastric mucosa of rats caused by duodenogastric reflux(DGR).Seventy-five healthy adult male SD rats were randomly divided into two groups:①DGR model group, 55 rats. They were classified into full reflux and partial reflux subgroups according to the ways of operative modelling and amounts of reflux; ②Sham operation group, 20 rats served as control group. Rat models were confirmed to be successful by monitoring pH and enzymatic estimation of total bile acid (TBA) in gastric juice. Dynamic observation on the damage of gastric mucosa in model rats was undertaken for 3～9 months after gastrojejunostomy.detect the expression of cyclin D 1 and p16 proteins in gastric mucosa with different lesions.The pH and TBA levels of gastric juice in DGR model group were significantly higher than those in control rats, showing success of DGR models. A dynamic progression of chronic superficial gastritis (CSG)→chronic atrophic gastritis (CAG)→dystopic hyperplasia (Dys) occurred in the pathological changes of model rats. The positive expression rates of cyclin D1 in CAG and Dys rats were significantly higher than those in CSG and control rats. There was no distinct difference in the expression of cyclin D 1 between CAG and Dys rats. On the contrary, the positive expression rate of suppressive oncogene p16 in control group was the highest as compared with the lowest results in Dys rats. Negative correlation was found between the expressions of cyclin D1 and p16.[Conclusion]The abnormal expression of cyclin D 1 and p16 gene proteins is one of the molecular mechanism in cell injury and canceration of gastric mucosa caused by DGR.
出处
《医学临床研究》
CAS
2004年第5期467-471,共5页
Journal of Clinical Research
基金
卫生部临床学科重点项目基金资助 (No .2 0 0 13 2 1)
关键词
十二指肠胃返流
胃粘膜
大鼠
基因
抑制
肿瘤
duodenogastric reflux
gastric mucosa
rats
genes,suppressor,tumor
