摘要
目的研究十二指肠胃反流(duodenogastric reflux,DGR)对大鼠胃黏膜细胞凋亡及相关细胞因子表达的影响,探讨DGR胃黏膜损伤机制。方法手术组成年SD大鼠10只用于制备和收集十二指肠混合液。DGR模型组和对照组各取SD大鼠8只,前者十二指肠液灌胃,后者生理盐水灌胃。2周后处死大鼠。采用TUNEL技术观察胃黏膜细胞凋亡情况。采用免疫组化方法分析胃黏膜组织TNF-α、ET-1和NOS-2的表达。结果 DGR模型大鼠胃黏膜病理提示造模成功。DGR模型组胃黏膜凋亡细胞在黏膜全层均可见,凋亡指数(AI)显著高于对照组(P<0.05)。DGR模型组大鼠胃黏膜细胞的TNF-α、ET-1和NOS-2的表达均明显高于对照组(P<0.05)。结论细胞凋亡与TNF-α、ET-1和NOS-2等细胞因子表达异常可能参与DGR胃黏膜损伤乃至细胞癌变的发病机制。
Objective To study on the gastric mucosal apoptosis and the expression of cell cytokines caused by duo- denogastric reflux （DGR） , and investigate the possible pathogenesis of gastric mucosa injury in rats with DGR. Methods Ten adult SD rats were intubated duodenum to collect duodenal mixed juice （including bile, pancreatic juice plus duodenal juice）. Another sixteen SD rats were randomly divided into two groups. The model group with DGR was trans- fused with duodenal mixed juice to stomach and the control group was transfused with 0.9% saline. The rats were exe- cuted after 14 days. Cell apoptosis in gastric mueosa was determined by TUNEL technique. Immunohistochemieal stai- ning was used to detect the expression of TNF-α, ET-1 and NOS-2 in gastric mucosa. Results The pathology of gastric mucosa demonstrated that rat models with DGR were successful. The apoptosis cells could be seen intensively in mucosa in DGR model group. Apoptosis index （AI） in DGR model group was significantly higher than that in control group （P 〈 0.05 ）. The positive expression of TNF-α, ET-1 and NOS-2 in DGR model group were significantly higher than those in control group （P 〈 0.05 ）. Conclusion Cell apoptosis and over expression of TNF-α, ET-1 and NOS-2 in gastric mucosa may be major pathogenesis of gastric mucosa injury and cell canceration with DGR.
出处
《胃肠病学和肝病学杂志》
CAS
2012年第6期533-535,540,共4页
Chinese Journal of Gastroenterology and Hepatology
